<?xml version="1.0" encoding="utf-8"?>
<XML>
<JOURNAL>
<YEAR>2022</YEAR>
<VOL>26</VOL>
<NO>1</NO>
<MOSALSAL>11</MOSALSAL>
<PAGE_NO>101</PAGE_NO>


<ARTICLES>

	<ARTICLE> 
		<TitleF>Anticonvulsant effects of squill oxymel (a traditional formulation) in mice</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: This study evaluated the anticonvulsant activity of the add-on Drimia maritima (squill) oxymel, used traditionally in the treatment of convulsion, in animal model. Methods: Albino mice pretreated with squill oxymel in different doses of 50, 100, 200 and 400mg/kg by oral gavage, 15min prior to injection of pentylenetetrazole (PTZ). Animals pretreated with flumazenil to determine the mechanism of anticonvulsant action. The total flavonoid content of squill oxymel was also determined. Results: Squill oxymel prolonged the onset of seizures and decreased the duration of seizures compared to control group. Diazepam used as a reference drug for its anticonvulsive effects, showed complete inhibition of seizure. This study revealed that squill oxymel has significant anticonvulsant effect in PTZ-induced seizures in mice and these effects may be related to its effect on benzodiazepines&#8217; receptors on GABA complex. Conclusion: These results confirmed the traditional use of squill oxymel in Iranian traditional medicine for treatment of epilepsy. The clarification of mechanisms involved needs further studies.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>1</FPAGE>
			<TPAGE>6</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/9
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/7/18
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/9
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1399/12/19
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Meysam</Name>
				<MidName></MidName>
				<Family>Abolmaali</Family>
				<NameE>Meysam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Abolmaali</FamilyE>
				<Organizations>
				<Organization>Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Manijeh</Name>
				<MidName></MidName>
				<Family>Motevalian</Family>
				<NameE>Manijeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Motevalian</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Saeed</Name>
				<MidName></MidName>
				<Family>Mehrzadi</Family>
				<NameE>Saeed</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mehrzadi</FamilyE>
				<Organizations>
				<Organization>Razi Drug Research Centre, Iran University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Asie</Name>
				<MidName></MidName>
				<Family>Shojaii</Family>
				<NameE>Asie</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Shojaii</FamilyE>
				<Organizations>
				<Organization>Department of Traditional Pharmacy, School of Persian Medicine, Iran University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>shojaii.a@iums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Drimia maritime</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Squill</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Oxymel</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Anticonvulsant</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Pentylenetetrazole</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Aghili Khorasani M., 1771. Makhzan-al-adviah (In Persian), edited by: Rahimi R, Farjadmand F, Shams Ardakani MR. Tehran University of medical sciences. 2009; 130-132.##Avicenna. The canon of Medicine. Tehran: Soroush Press, 2008.##Belhaddad OE, Charef N, Amamra S, Zerargui F, Baghiani A, Khennouf S, et al. Chromatographic fractionation, antioxidant and antibacterial activities of Urginea maritima methanolic extract. Pak J Pharm Sci 2018. 30: 127-34##Bozorgi M, Amin G, Shekarchi M, Rahimi R. Traditional medical uses of Drimia species in terms of phytochemistry, pharmacology and toxicology. J Tradit Chin Med 2017; 37: 124-39.##Chamberlain FL, Levy RL. Clinical study of a preparation of squill (urginin) in the treatment of myocardial insufficiency. Am Heart J 1937; 14: 268-83.##Corda M, Giorgi O, Longoni B, Orlandi M, Biggio G. Decrease in the function of the γ‐aminobutyric acid‐ coupled chloride channel produced by the repeated administration of pentylenetetrazol to rats. J Neurochem 1990; 55: 1216-21.##Dizaye KF, Hamad BA. Cardiovascular studies of white squill (Urginea maritima) extract. Zanco J Med Sci 2010; 14: 20-7.##Greenberg AE. Standard methods for the examination of water and wastewater. Washington DC, American Public Health Association. 1981.##Haile M, Kang WH. Antioxidant activity, total polyphenol, flavonoid and tannin contents of fermented green coffee beans with selected yeasts. Fermentation 2019; 5: 29.##Johannessen Landmark C, Patsalos PN. Drug interactions involving the new second- and third-generation antiepileptic drugs. Expert Rev Neurother 2010; 10: 119-40.##Kirmani BF, Robinson DM, Kikam A, Fonkem E, Cruz D. Selection of antiepileptic drugs in older people. Curr Treat Options Neurol 2014; 16: 295.##Mammadov R, Makasçı-Afacan A, Uysal-Demir D, Görk Ç. Determination of antioxidant activities of different Urginea maritima (L.) Baker plant extracts. Iranian Journal of Chemistry and Chemical Engineering (IJCCE) 2010; 29: 47-53.##Mehrzadi S, Sadr S, Hosseinzadeh A, Gholamine B, Shahbazi A, FallahHuseini H, et al. Anticonvulsant activity of the ethanolic extract of Punica granatum L. seed. Neurol Res 2015; 37: 470-5.##Mehrzadi S, Shojaii A, Pur SA, Motevalian M. Anticonvulsant activity of hydroalcoholic extract of Citrullus colocynthis fruit: involvement of benzodiazepine and opioid receptors. Evid-Based Compl Alt 2016; 21: 31-5.##Moshi MJ, Kagashe GA, Mbwambo ZH. Plants used to treat epilepsy by Tanzanian traditional healers. J Ethnopharmacol 2005; 97: 327-36.##Motevalian M, Mehrzadi S, Ahadi S, Shojaii A. Anticonvulsant activity of Dorema ammoniacum gum: evidence for the involvement of benzodiazepines and opioid receptors. Res Pharm Sci 2017; 12: 53-9.##Nejatbakhsh F, Karegar-Borzi H, Amin G, Eslaminejad A, Hosseini M, Bozorgi M, et al. Squill Oxymel, a traditional formulation from Drimia Maritima (L.) Stearn, as an add-on treatment in patients with moderate to severe persistent asthma: A pilot, triple-blind, randomized clinical trial. J Ethnopharmacol 2017; 196: 186-92.##Ngugi AK, Bottomley C, Kleinschmidt I, Sander JW, Newton CR. Estimation of the burden of active and life-time epilepsy: a meta-analytic approach. Epilepsia 2010; 51: 883-90.##Obeidat M, Sharab A. Antimicrobial and anticancer activities of extracts from Urginea maritime fruits. Afr J Tradit Complement Altern Med 2018; 15: 74-84.##Rashidian A, Farhang F, Vahedi H, Dehpour AR, Ejtemai Mehr S, Mehrzadi S, et al. Anticonvulsant effects of Lippia citriodora (Verbenaceae) leaves ethanolic extract in mice: role of GABAergic system. Int J Prev Med 2016; 7: 97.##Rashidian A, Kazemi F, Mehrzadi S, Dehpour AR, Mehr SE, Rezayat SM. Anticonvulsant effects of aerial parts of verbena officinalis extract in mice: involvement of benzodiazepine and opioid receptors. J Evid Based Complementary Altern Med 2017; 22: 632-6.##Riazi K, Honar H, Homayoun H, Rashidi N, Dehghani M, Sadeghipour H, et al. Sex and estrus cycle differences in the modulatory effects of morphine on seizure susceptibility in mice. Epilepsia 2004; 45: 1035-42.##Shahidi F, Ho CT. Antioxidant measurement and applications: an overview. J Am Chem Soc 2007: 2-7.##Shams Ardakani MR, Farjadmand F, Rahimi R. Makhzan al Adviyeh and Pointing to the Scientific Names of Medicinal Plants for the First Time in a Persian Book. Trad Integr Med. 3(4):186-195.##Stannard J. Squill in ancient and medieval materia medica, with special reference to its employment for dropsy. Bull N Y Acad Med 1974; 50: 684-713.##Thurman DJ, Beghi E, Begley CE, Berg AT, Buchhalter JR, Ding D, et al. Standards for epidemiologic studies and surveillance of epilepsy. Epilepsia 2011; 52: 2-26.##Zargari A. Medicinal plants. Tehran: Tehran University of medical sciences publication, 1996.##Zhu HL, Wan JB, Wang YT, Li BC, Xiang C, He J, et al. Medicinal compounds with antiepileptic/anticonvulsant activities. Epilepsia 2014; 55: 3-16.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Enriched-asafoetida diet attenuates hyperglycemia, oxidative stress and endothelial dysfunction in type 2 diabetic rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: It has been documented that oxidative stress and inflammation are the main causes of diabetic-induced disorders. Several studies have been reported the antioxidant and antidiabetic effects of prepared asafoetida extracts, from Ferula assafoetida L. species in the Apiaceae family. The aim of the present study was to evaluate the effects of enriched-asafoetida diet (EAD) 0.5% and 2% on plasma level of glucose, hemoglobin A1C (HbA1C), insulin, lipid profile and hepatic enzymes, and vascular endothelial dysfunction induced by type 2 diabetes (T2D). Methods: Thirty-two male Wistar rats were divided into four groups: 1) control group, 2) diabetic group, 3 and 4) diabetic groups received EAD0.5% and EAD2% for 4 weeks, respectively. T2D was induced by intraperitoneal injection of nicotinamide and streptozotocin. At the end of the experiment, the plasma level of glucose, lipid profile, insulin, oxidative stress, hepatic enzymes and vascular dysfunction were evaluated. Results: Fasting blood sugar, HbA1C, oxidative stress and hepatic enzymes significantly decreased and plasma level of insulin markedly increased in the EAD0.5 compared to the diabetic group. The plasma lipid profile was improved in the EAD0.5 group. The response of thoracic aorta rings to vasodilators and vasoconstrictor substances was considerably improved in EAD0.5 than in the diabetic group. The EAD2 did not have a significant effect on diabetic induced disorders. Conclusion: The results of the present study suggest that the effects of EAD on biological disorders caused by T2D are dependent on the percentage of asafoetida in the diet.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>7</FPAGE>
			<TPAGE>19</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/23
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/11/4
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/10
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/21
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mansour</Name>
				<MidName></MidName>
				<Family>Esmailidehaj</Family>
				<NameE>Mansour</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Esmailidehaj</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>med1354@ssu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahboobe</Name>
				<MidName></MidName>
				<Family>Kahtenaroon</Family>
				<NameE>Mahboobe</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Kahtenaroon</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad Ebrahim</Name>
				<MidName></MidName>
				<Family>Rezvani</Family>
				<NameE>Mohammad Ebrahim</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rezvani</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Hossein</Name>
				<MidName></MidName>
				<Family>Azizian</Family>
				<NameE>Hossein</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Azizian</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Alimohammad</Name>
				<MidName></MidName>
				<Family>Ranjbar</Family>
				<NameE>Alimohammad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ranjbar</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacognosy, School of Pharmacy Shahid Sadoughi University of Medical Sciences, Yazd, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Type 2 diabetes</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Asafoetida</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Hemoglobin A1C</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Vascular dysfunction</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Lipid profile.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Abu-Zaiton AS. Anti-diabetic activity of Ferula assafoetida extract in normal and alloxan-induced diabetic rats. Pakistan J Biol Sci. 2010;13:97–100. https://dx.doi.org/10.3923/pjbs.2010.97.100##Al-Awadi F, Shoukry M. The lipid lowering effect of an anti-diabetic plant extract. Acta Diabetol Lat 1988; 25: 1–5.##Amalraj A, Gopi S. Biological activities and medicinal properties of Asafoetida: A review. Journal of Traditional and Complementary Medicine. 2017; 7: 347–359.##Ayoubi A, Arshami J, Valizadeh R, Mousavi Z, Mousaei A. The Effect of Asafetida Gum Extract on Blood Parameters and Histopathology of Testes in Male Wistar Rat. Iran J Anim Sci Res. 2013;4:310–5.##Azizian H, Rezvani ME, Esmaeilidehaj M, Bagheri SM. Anti-Obesity, Fat Lowering and Liver Steatosis Protective Effects of Ferula asafoetida Gum in Type 2 Diabetic Rats: Possible Involvement of Leptin. Iran J Diabetes Obes. 2012;4:120–6.##Brodsky IG. Nutritional effects of dietary protein restriction in insulin-dependent diabetes mellitus. In: Journal of Nutrition. 1998;128:2Sup.##Castedo E, Segovia J, Escudero C, Olmedilla B, Granado F, Blas C, et al. Ischemia-Reperfusion Injury During Experimental Heart Transplantation. Evaluation of Trimetazidine’s Cytoprotective Effect. Rev Española Cardiol (English Ed). 2005; 58: 941–950.##Chandran S, Sakthivel M, Thirumavalavan M, Thota JR, Mariappanadar V, Raman P. A facile approach to the isolation of proteins in Ferula asafoetida and their enzyme stabilizing, anti-microbial and anti-oxidant activity. Int J Biol Macromol. 2017; 102: 1211–1219.##Chukwuma CI, Matsabisa MG, Ibrahim MA, Erukainure OL, Chabalala MH, Islam MS. Medicinal plants with concomitant anti-diabetic and anti-hypertensive effects as potential sources of dual acting therapies against diabetes and hypertension: A review. J Ethnopharmacol 2019; 235: 329–360.##Dehpour AA, Ebrahimzadeh MA, Fazel NS, Mohammad NS. Antioxidant activity of the methanol extract of Ferula assafoetida and its essential oil composition. Grasas y Aceites. 2009; 60: 405–412.##Esmaeili H, Sharifi M, Esmailidehaj M, Rezvani ME, Hafizibarjin Z. Vasodilatory effect of asafoetida essential oil on rat aorta rings: The role of nitric oxide, prostacyclin, and calcium channels. Phytomedicine. 2017; 36: 88–94.##Esmailidehaj M, khaje bahabadi Z, Rezvani ME. Investigating the Effect of Oral Consumption of Tear Assafoetida on Hepatic, Renal, Cardiac, and Blood Biochemical Parameters of Rats. J Shahid Sadoughi Univ Med Sci. 2013;21:641–50.##Esmailidehaj M, Rezvani ME, Mosaddeghmehrjardi MH. Pretreatment with Assafoetida exerts dose-dependent dual effects on rat hearts. Pharmacogn Mag. 2014; 10: 147–153.##Fararh KM, Atoji Y, Shimizu Y, Takewaki T. Isulinotropic properties of Nigella sativa oil in Streptozotocin plus nicotinamide diabetic hamster. Res Vet Sci 2002; 73: 279–282.##Giugliano D, Ceriello A, Esposito K. Glucose metabolism and hyperglycemia. In: American Journal of Clinical Nutrition. 2008;87:1.##Harris EH. Elevated liver function tests in type 2 diabetes. Clin Diabetes 2005; 23: 115–119.##Hejazian S, Dashti-R M, Bagheri S. The Relaxant Effect of Seed′s Essential Oil and Oleo-gum-resin of Ferula Assa-foetida on Isolated Rat′s Ileum. Ann Med Health Sci Res. 2014;4:238.##Hink U, Li H, Mollnau H, Oelze M, Matheis E, Hartmann M, et al. Mechanisms underlying endothelial dysfunction in diabetes mellitus. Circ Res. 2001;88:e14-22.##Howlett J, Ashwell M. Glycemic response and health: Summary of a workshop. Am J Clin Nutr. 2008;87.##Huebschmann AG, Regensteiner JG, Vlassara H, Reusch JEB. Diabetes and advanced glycoxidation end products. Diabetes Care. 2006;29:1420–32.##Husna F, Suyatna FD, Arozal W, Poerwaningsih EH. Anti-Diabetic Potential of Murraya Koenigii (L) and its Antioxidant Capacity in Nicotinamide-Streptozotocin Induced Diabetic Rats. Drug Res (Stuttg). 2018;68:631–6.##Iranshahy M, Iranshahi M. Traditional uses, phytochemistry and pharmacology of asafoetida (Ferula assa-foetida oleo-gum-resin) - A review. Journal of Ethnopharmacology. 2011; 134: 1–10.##Kasaian J, Asili J, Iranshahi M. Sulphur-containing compounds in the essential oil of Ferula alliacea roots and their mass spectral fragmentation patterns. Pharm Biol. 2016;54:2264–8.##Kasetti RB, Rajasekhar MD, Kondeti VK, Fatima SS, Kumar EGT, Swapna S, et al. Antihyperglycemic and antihyperlipidemic activities of methanol:water (4:1) fraction isolated from aqueous extract of Syzygium alternifolium seeds in streptozotocin induced diabetic rats. Food Chem Toxicol. 2010;48:1078–84.##Kiyanmehr M, Boskabady MH, Khazdair MR, Hashemzehi M. Possible mechanisms for functional antagonistic effect of Ferula assafoetida on muscarinic receptors in tracheal smooth muscle. Malaysian J Med Sci. 2016; 23: 35–43##Kolluru GK, Bir SC, Kevil CG. Endothelial dysfunction and diabetes: Effects on angiogenesis, vascular remodeling, and wound healing. International Journal of Vascular Medicine. 2012.##Krishna Kundu N, Obayed Ullah M, Hamid K, Urmi KF, Bulbul IJ, Khan MAI, et al. Studies of lipid profile, liver function and kidney function parameters of rat plasma after chronic administration of “Sulavajrini Vatika.” Pakistan J Biol Sci. 2012;15:666–72.##Kristová V, Líšková S, Sotníková R, Vojtko R, Kurtanský A. Sulodexide improves endothelial dysfunction in streptozotocin-induced diabetes in rats. Physiol Res. 2008; 57: 491–494.##Latifi E, Mohammadpour AA, H BF, Nourani H. Antidiabetic and antihyperlipidemic effects of ethanolic Ferula assa-foetida oleo-gum-resin extract in streptozotocin-induced diabetic wistar rats. Biomed Pharmacother. 2019;110:197–202.##Lee CL, Chiang LC, Cheng LH, Liaw CC, Abd El-Razek MH, Chang FR, et al. Influenza A (H1N1) antiviral and cytotoxic agents from Ferula assa-foetida. J Nat Prod. 2009;72:1568–72.##Mahendra P, Bisht S. Ferula asafoetida : Traditional uses and pharmacological activity. Pharmacogn Rev. 2012;6:141–6.##Mallikarjuna GU, Dhanalakshmi S, Raisuddin S, Ramesha Rao A. Chemomodulatory Influence of Ferula asafoetida on Mammary Epithelial Differentiation, Hepatic Drug Metabolizing Enzymes, Antioxidant Profiles and N-methyl-N-Nitrosourea-Induced Mammary Carcinogenesis in Rats. Breast Cancer Res Treat. 2003;81:1–10.##Mitchell JA, Ali F, Bailey L, Moreno L, Harrington LS. Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium. In: Experimental Physiology. 2008; 93: 141–147.##Nishikawa T, Edelstein D, Du XL, Yamagishi SI, Matsumura T, Kaneda Y, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature. 2000; 404: 787–790.##O’Brien RM, Granner DK. Regulation of gene expression by insulin. Physiol Rev. 1996;76:1109–61.##Palsamy P, Subramanian S. Resveratrol, a natural phytoalexin, normalizes hyperglycemia in streptozotocin-nicotinamide induced experimental diabetic rats. Biomed Pharmacother. 2008; 62: 598–605.##Pari L, Sankaranarayanan C. Beneficial effects of thymoquinone on hepatic key enzymes in streptozotocin-nicotinamide induced diabetic rats. Life Sci. 2009;85:830–4.##Patel DK, Kumar R, Laloo D, Hemalatha S. Diabetes mellitus: An overview on its pharmacological aspects and reported medicinal plants having antidiabetic activity. Asian Pacific Journal of Tropical Biomedicine. 2012; 2: 411–420.##Pepato MT, Migliorini RH, Goldberg AL, Kettelhut IC. Role of different proteolytic pathways in degradation of muscle protein from streptozotocin-diabetic rats. Am J Physiol - Endocrinol Metab. 1996; 271.##Sharma B, Balomajumder C, Roy P. Hypoglycemic and hypolipidemic effects of flavonoid rich extract from Eugenia jambolana seeds on streptozotocin induced diabetic rats. Food Chem Toxicol. 2008;46:2376–83.##Shivashankara AR, Azmidah A, Haniadka R, Rai MP, Arora R, Baliga MS. Dietary agents in the prevention of alcohol-induced hepatotoxicty: Preclinical observations. Food Funct. 2012;3:101–9.##Soni KB, Rajan A, Kuttan R. Inhibition of aflatoxin-induced liver damage in ducklings by food additives. Mycotoxin Res. 1993;9:22–6.##Sotnikova R, Okruhlicova L, Vlkovicova J, Navarova J, Gajdacova B, Pivackova L, et al. Rosmarinic acid administration attenuates diabetes-induced vascular dysfunction of the rat aorta. J Pharm Pharmacol. 2013;65:713–23.##Taylor SG, Southerton JS, Weston AH, Baker JRJ. Endothelium‐dependent effects of acetylcholine in rat aorta: a comparison with sodium nitroprusside and cromakalim. Br J Pharmacol. 1988;94:853–63.##Wold LE, Ceylan-Isik AF, Ren J. Oxidative stress and stress signaling: Menace of diabetic cardiomyopathy. Acta Pharmacol Sin. 2005;26:908–17.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Naringin ameliorates cognitive impairment in streptozotocin/nicotinamide induced type 2 diabetes in Wistar rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Psychomotor slowing and reduced mental flexibility are symptoms of cognitive decline that can occur in type 2 diabetes disease (TD2). Strategies that combine the control of hyperglycaemia with prevention of cognitive decline are desirable. Thus, this study reports the effect of naringin on cognitive deficit in diabetic rats. Methods: TD2 in Wistar rats was induced with nicotinamide/streptozotocin (NA/STZ). Naringin (50 and 100 mg/kg) or glibenclamide (5mg/kg) was administered for 30 days to diabetic rats. Cognitive performance was investigated using the Morris water maze. Serum glucose, lipid profiles, brain tumour necrosis factor alpha (TNF-&#945;) and acetylcholinesterase (AChE) activity were determined. Results: Naringin and glibenclamide significantly reduced the escape latency, increased the time spent in the correct quadrant and number of entries in diabetic rats. Also, naringin reduced blood glucose, serum cholesterol, low-density lipoprotein cholesterol levels, triglycerides and prevented a decrease in the level of high-density lipoprotein cholesterol, in diabetic rats. Naringin and glibenclamide treated diabetic rats showed a significant low levels of AChE activity and TNF-&#945;. Conclusion: Naringin ameliorates diabetes induced cognitive deficit via reduction of inflammation, hyperglycemia, hyperlipidaemia and AChE activity</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>20</FPAGE>
			<TPAGE>29</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/12
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/2/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Abiodun</Name>
				<MidName></MidName>
				<Family>Oyindamola O</Family>
				<NameE>Abiodun</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Oyindamola O</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country>Nigeria</Country>
				</Countries>
				<EMAILS>
				<Email>oo.abiodun@mail.ui.edu.ng</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Bakre</Name>
				<MidName></MidName>
				<Family>Adewale G</Family>
				<NameE>Bakre</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Adewale G</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country>Nigeria</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Adekoya</Name>
				<MidName></MidName>
				<Family>Christiana T</Family>
				<NameE>Adekoya</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Christiana T</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country>Nigeria</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Kazeem</Name>
				<MidName></MidName>
				<Family>Adebola I</Family>
				<NameE>Kazeem</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Adebola I</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country>Nigeria</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Oke</Name>
				<MidName></MidName>
				<Family>Tolulope A</Family>
				<NameE>Oke</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Tolulope A</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Ibadan, Ibadan, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country>Nigeria</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ujomu</Name>
				<MidName></MidName>
				<Family>Tejumade S</Family>
				<NameE>Ujomu</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Tejumade S</FamilyE>
				<Organizations>
				<Organization>Department of Anatomy, Physiology and Pharmacology, Lead City University, Ibadan, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country>Nigeria</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Naringin</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Diabetes</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Cognitive decline</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Inflammation</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Acetylcholinesterase.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Adil M, Visnagri A, Kumar VS, Kandhare AD, Ghosh P, Bodhankar S. Protective effect of naringin on sodium arsenite induced testicular toxicity via modulation of biochemical perturbations in experimental rats. Pharmacologia 2014; 5: 222-34.##Ahmad W, Singh S, Kumar S. Phytochemical screening and antimicrobial study of Euphorbia hirta extracts. J Med Plants Stud 2017; 5: 183-86.##Ahmed OM, Hassan MA, Abdel-Twab S M, Azeem MN. Navel orange peel hydroethanolic extract, naringin and naringenin have anti-diabetic potentials in type 2 diabetic rats. Biomed Pharmacother 2017; 94: 197-205.##Baynes HW. Classification, pathophysiology, diagnosis and management of diabetes mellitus. J diabetes metab 2015; 6: 1-9.##Benavente-Garcia O, Castillo J. Update on uses and properties of citrus flavonoids: new findings in anticancer, cardiovascular, and anti-inflammatory activity. J Agric Food Chem 2008; 56: 6185-205.##Biessels G, Kappelle L. Utrecht Diabetic Encephalopathy Study G. Increased risk of Alzheimer's disease in Type II diabetes: insulin resistance of the brain or insulin-induced amyloid pathology. Biochem Soc Trans 2005; 33: 1041-4.##Bok SH, Shin YW, Bae KH, Jeong TS, Kwon YK, Park YB, et al. Effects of naringin and lovastatin on plasma and hepatic lipids in high-fat and high-cholesterol fed rats. Nutr Res 2000; 20: 1007-15.##Brands MW, Bell TD, Gibson B. Nitric oxide may prevent hypertension early in diabetes by counteracting renal actions of superoxide. Hypertension 2004; 43: 57-63.##Bromley-Brits K, Deng Y, Song W. Morris water maze test for learning and memory deficits in Alzheimer's disease model mice. J Vis Exp 2011; 53: e2920.##Carvajal FJ, Inestrosa NC. Interactions of AChE with Aβ aggregates in Alzheimer's brain: therapeutic relevance of IDN 5706. Front Mol Neurosci 2011; 4: 19.##Chen F, Zhang N, Ma X, Huang T, Shao Y, Wu C, et al. Naringin alleviates diabetic kidney disease through inhibiting oxidative stress and inflammatory reaction. Plos One 2015; 10: e0143868.##Chen Y, Nie YC, Luo YL, Lin F, Zheng YF, Cheng GH, et al. Protective effects of naringin against paraquat-induced acute lung injury and pulmonary fibrosis in mice. Food Chem Toxicol 2013; 58: 133-40.##Choe SC, Kim HS, Jeong TS, Bok SH, Park YB. Naringin has an antiatherogenic effect with the inhibition of intercellular adhesion molecule-1 in hypercholesterolemic rabbits. J Cardiovasc Pharmacol 2001; 38: 947-55.##Craft S, Cholerton B, Baker LD. Insulin and Alzheimer's disease: untangling the web. J Alzheimers Dis 2013; 33: 263-75.##Dodel R, Rominger A, Bartenstein P, Barkhof F, Blennow K, Förster S, et al. Intravenous immunoglobulin for treatment of mild-to-moderate Alzheimer's disease: a phase 2, randomised, double-blind, placebo-controlled, dose-finding trial. Lancet Neurol 2013; 12: 233-43.##Duarte JM. Metabolic alterations associated to brain dysfunction in diabetes. Aging Dis 2015; 6: 304-21.##Ellman GL, Courtney KD, Andres Jr V, Featherstone RM. A new and rapid colorimetric determination of acetylcholinesterase activity. Biochem Pharmacol 1961; 7: 88-95.##Friedwald W, Leve R, Fredrichson D. Estimation of concentration of low density lipoproteins separated by three different methods. Clin Chem 1972; 18: 499-502.##Haam J, Yakel JL. Cholinergic modulation of the hippocampal region and memory function. J Neurochem 2017; 142: 111-21.##Jung UJ, Lee MK, Jeong KS, Choi MS. The hypoglycemic effects of hesperidin and naringin are partly mediated by hepatic glucose-regulating enzymes in C57BL/KsJ-db/db mice. J Nutr 2004; 134: 2499-503.##Jung UJ, Lee MK, Park YB, Kang MA, Choi MS. Effect of citrus flavonoids on lipid metabolism and glucose-regulating enzyme mRNA levels in type-2 diabetic mice. Int J Biochem Cell Biol 2006; 38: 1134-45.##Kloppenborg RP, van den Berg E, Kappelle LJ, Biessels GJ. Diabetes and other vascular risk factors for dementia: which factor matters most? A systematic review. Eur J Pharmacol 2008; 585: 97-108.##Kopf SR, Baratti CM. Effects of posttraining administration of insulin on retention of a habituation response in mice: participation of a central cholinergic mechanism. Neurobiol Learn Mem 1999; 71: 50-61.##Lin CY, Ni CC, Yin MC, Lii CK. Flavonoids protect pancreatic beta-cells from cytokines mediated apoptosis through the activation of PI3-kinase pathway. Cytokine 2012; 59: 65-71.##Liu X, Liu M, Mo Y, Peng H, Gong J, Li Z, et al. Naringin ameliorates cognitive deficits in streptozotocin-induced diabetic rats. Iran J Basic Med Sci 2016; 19: 417-22.##Madsen PA, Bingham H, Liu H. A new Boussinesq method for fully nonlinear waves from shallow to deep water. J Fluid Mech 2002; 462: 1-33.##Masiello P, Broca C, Gross R, Roye M, Manteghetti M, Hillaire-Buys D, et al. Experimental NIDDM: development of a new model in adult rats administered streptozotocin and nicotinamide. Diabetes 1998; 47: 224-29.##Morris RG. Spatial localization does not require the presence of local cues. Learn Motiv 1981; 12: 239-60.##Mushtaq M, Sultana B, Bhatti HN, Asgher M. Optimization of enzyme-assisted revalorization of sweet lime (Citrus limetta Risso) peel into phenolic antioxidants. BioResources 2014; 9: 6153- 65.##Namas R, Ghuma A, Hermus L, Zamora R, Okonkwo D, Billiar T, et al. The acute inflammatory response in trauma/hemorrhage and traumatic brain injury: current state and emerging prospects. Libyan J Med 2009; 4: 97-103.##Owira PM, Ojewole JA. The grapefruit: an old wine in a new glass? Metabolic and cardiovascular perspectives. Cardiovasc J Afr 2010; 21: 280-85.##Pollack RM, Donath MY, LeRoith D, Leibowitz G. Anti-inflammatory agents in the treatment of diabetes and its vascular complications. Diabetes care 2016; 39: 244-252.##Rajadurai M, Prince PS. Preventive effect of naringin on isoproterenol-induced cardiotoxicity in Wistar rats: an in vivo and in vitro study. Toxicology 2007; 232: 216-25.##Ribeiro IA, Ribeiro MH. Naringin and naringenin determination and control in grapefruit juice by a validated HPLC method. Food Control 2008; 19: 432-38.##Rosen DR, Siddique T, Patterson D, Figlewicz DA, Sapp P, Hentati A, et al. Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis. Nature 1993; 362: 59-62.##Saelens W, Cannoodt R, Todorov H, Saeys Y. A comparison of single-cell trajectory inference methods. Nat Biotechnol 2019; 37: 547-54.##Sima AA. Encephalopathies: the emerging diabetic complications. Acta Diabetol 2010; 47: 279- 93.##Singh D, Chopra K. The effect of naringin, a bioflavonoid on ischemia-reperfusion induced renal injury in rats. Pharmacol Res 2004; 50: 187-93.##Stephens JM, Lee J, Pilch PF. Tumor necrosis factor-α-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. J Biol Chem 1997; 272: 971-76.##Wang X, Liu H, Zhang Y, Li J, Teng X, Liu A, et al. Effects of isolated positive maternal thyroglobulin antibodies on brain development of offspring in an experimental autoimmune thyroiditis model. Thyroid 2015; 25: 551-8.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The impact of sesamol and exercise on striatal TNF-α level, motor behavior, aversive memory and oxidative stress status in 6-hydroxydopamine-lesioned rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Neuroinflammation and oxidative stress play critical roles in the pathophysiology of Parkinson&#8217;s disease (PD), and neuroprotective agents could be helpful to slow down the dopaminergic neurodegeneration. Neuroprotective and antioxidant properties of exercise and sesamol have been previously reported. The current research evaluated the influences of sesamol and exercise on memory and motor impairments, oxidative stress and inflammatory markers in an experimental model of PD. Methods: 6-hydroxydopamine (6-OHDA) was microinjected into the medial forebrain bundle of male rats. Treatment with sesamol (50mg/kg) or treadmill exercise was performed for 7 weeks. Behavioral and biochemical assessments were performed at the end of 6th week after 6-OHDA injection. Results: Net number of rotations and tumor necrosis factor (TNF)-&#945; level was significantly enhanced in 6-OHDA group in comparison with sham group. Also, step-through latency was decreased in this group along with increased lipid peroxidation and decreased total thiol levels in the hippocampus. Moreover, sesamol and exercise, alone or in combination, improved rotational behavior, which was accompanied by decreased striatal TNF-&#945; level. However, sesamol and/or treadmill exercise had no effect on aversive memory, although exercise enhanced hippocampal total thiol level. Conclusion: Beneficial properties of sesamol and treadmill exercise for amelioration of motor impairments might be due to their anti-inflammatory activities.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>30</FPAGE>
			<TPAGE>38</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/19
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/9/29
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/10
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/21
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Somayeh</Name>
				<MidName></MidName>
				<Family>Shahidani</Family>
				<NameE>Somayeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Shahidani</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ziba</Name>
				<MidName></MidName>
				<Family>Rajaei</Family>
				<NameE>Ziba</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rajaei</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>rajaeiz@med.mui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Hojjatallah</Name>
				<MidName></MidName>
				<Family>Alaei</Family>
				<NameE>Hojjatallah</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Alaei</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>alaei@med.mui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Samaneh</Name>
				<MidName></MidName>
				<Family>Mohammadzadeh</Family>
				<NameE>Samaneh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mohammadzadeh</FamilyE>
				<Organizations>
				<Organization>Poursina Hakim Digestive Diseases Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Sesamol</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>6-OHDA</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Exercise</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Motor activity</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Memory</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Oxidative stress.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Aguiar AS, Speck AE, Prediger RD, Kapczinski F, Pinho RA. Downhill training upregulates mice hippocampal and striatal brain-derived neurotrophic factor levels. J Neural Transm 2008; 115: 1251-5.##Aguiar AS, Tristão FSM, Amar M, Chevarin C, Glaser V, de Paula Martins R, et al. Six weeks of voluntary exercise don't protect C57BL/6 mice against neurotoxicity of MPTP and MPP+. Neurotox Res 2014; 25: 147-52.##Bjørklund G, Peana M, Maes M, Dadar M, Severin B. The glutathione system in Parkinson's disease and its progression. Neurosci Biobehav Rev 2021; 120: 470-8.##Campos FL, Carvalho MM, Cristovão AC, Je G, Baltazar G, Salgado AJ, et al. Rodent models of Parkinson's disease: beyond the motor symptomatology. Front Behav Neurosci 2013; 7: 175.##Chopra K, Tiwari V, Arora V, Kuhad A. Sesamol suppresses neuro-inflammatory cascade in experimental model of diabetic neuropathy. J Pain 2010; 11: 950-7.##Cicchetti F, Brownell A, Williams K, Chen Y, Livni E, Isacson O. Neuroinflammation of the nigrostriatal pathway during progressive 6‐OHDA dopamine degeneration in rats monitored by immunohistochemistry and PET imaging. Eur J Neurosci 2002; 15: 991-8.##Dexter DT, Jenner P. Parkinson disease: from pathology to molecular disease mechanisms. Free Radic Biol Med 2013; 62: 132-44.##Getz SJ, Levin B. Cognitive and neuropsychiatric features of early Parkinson's disease. Arch Clin Neuropsychol 2017; 32: 769-85.##Goodwin VA, Richards SH, Taylor RS, Taylor AH, Campbell JL. The effectiveness of exercise interventions for people with Parkinson's disease: A systematic review and meta‐analysis. Mov Disord 2008; 23 :631-40.##Haddadi H, Rajaei Z, Alaei H, Shahidani S. Chronic treatment with carvacrol improves passive avoidance memory in a rat model of Parkinson's disease. Arq Neuropsiquiatr 2018; 76: 71-7.##Hamzehloei L, Rezvani ME, Rajaei Z. Effects of carvacrol and physical exercise on motor and memory impairments associated with Parkinson's disease. Arq Neuropsiquiatr 2019; 77: 493- 500.##Hanrott K, Gudmunsen L, O'Neill MJ, Wonnacott S. 6-hydroxydopamine-induced apoptosis is mediated via extracellular auto-oxidation and caspase 3-dependent activation of protein kinase Cδ. J Biol Chem 2006; 281: 5373-82.##Hirsch EC, Hunot S. Neuroinflammation in Parkinson's disease: A target for neuroprotection? Lancet Neurol 2009; 8: 382-97.##Hosseini H, Rajaei Z, Alaei H, Tajadini M. The effects of crocin on 6-OHDA-induced oxidative/nitrosative damage and motor behaviour in hemiparkinsonian rats. Malays J Med Sci 2016; 23: 35-43.##Hsu DZ, Chien SP, Chen KT, Liu MY. The effect of sesamol on systemic oxidative stress and hepatic dysfunction in acutely iron-intoxicated mice. Shock 2007; 28: 596-601.##Khadira Sereen A, Vijayalakshmi K, Nagappan P, Balima S. Effect of sesamol in association with folic acid on 6-OHDA induced parkinsonian animals-biochemical, neurochemical and histopathological evidence. Asian J Clin Res 2017; 10: 46-50.##Kuhad A, Chopra K. Effect of sesamol on diabetes-associated cognitive decline in rats. Exp Brain Res 2008; 185: 411-20.##Kumar P, Kalonia H, Kumar A. Sesamol attenuate 3-nitropropionic acid-induced Huntingtonlike behavioral, biochemical, and cellular alterations in rats. J Asian Nat Prod Res 2009; 11: 439- 50.##Kumar P, Kalonia H, Kumar A. Protective effect of sesamol against 3-nitropropionic acidinduced cognitive dysfunction and altered glutathione redox balance in rats. Basic Clin Pharmacol Toxicol 2010; 107: 577-82.##Lang AE, Lozano AM. Parkinson disease, first of two parts. N Engl J Med 1998; 339: 1044-53.##Lee JK, Tran T, Tansey MG. Neuroinflammation in Parkinson's disease. J Neuroimmune Pharmacol 2009; 4: 419-29.##Lee HJ, Kim C, Lee SJ. Alpha-synuclein stimulation of astrocytes: potential role for neuroinflammation and neuroprotection. Oxid Med Cell Longev 2010; 3.##Long-Smith CM, Sullivan AM, Nolan YM. The influence of microglia on the pathogenesis of Parkinson's disease. Prog Neurobiol 2009; 89: 277-87.##Macêdo PFCd, de Melo JSV, Costa LAR, Braz GRF, de Sousa SM, Lagranha CJ, et al. Fish oil and treadmill exercise have age-dependent effects on episodic memory and oxidative state of the hippocampus. Appl Physiol Nutr Metab 2017; 42: 503-10.##Mokry J. Experimental models and behavioural tests used in the study of Parkinson's disease. Physiol Res 1995; 44: 143-50.##Nagatsu T, Sawada M. Inflammatory process in Parkinson's disease: role for cytokines. Curr Pharm Design 2005; 11: 999-1016.##Niranjan R. The role of inflammatory and oxidative stress mechanisms in the pathogenesis of Parkinson's disease: focus on astrocytes. Mol Neurobiol 2014; 49: 28-38.##Parihar VK, Prabhakar K, Veerapur VP, Kumar MS, Reddy YR, Joshi R, et al. Effect of sesamol on radiation-induced cytotoxicity in Swiss albino mice. Mutat Res-Gen Tox Environ Mutat 2006; 611: 9-16.##Paxinos G, Watson C. The rat brain in stereotaxic coordinates. Burlington (MA). San Diego (CA), London (UK): Elsevier Academic Press; 2005.##Pieper HC, Evert BO, Kaut O, Riederer PF, Waha A, Wüllner U. Different methylation of the TNF-alpha promoter in cortex and substantia nigra: implications for selective neuronal vulnerability. Neurobiol Dis 2008; 32: 521-7.##Prasad NR, Mahesh T, Menon VP, Jeevanram R, Pugalendi KV. Photoprotective effect of sesamol on UVB-radiation induced oxidative stress in human blood lymphocytes in vitro. Environ Toxicol Pharmacol 2005; 20: 1-5.##Qian L, Flood PM, Hong JS. Neuroinflammation is a key player in Parkinson's disease and a primetarget for therapy. J Neural Transm 2010; 117: 971-9.##Rajaei Z, Hosseini M, Alaei H. Effects of crocin on brain oxidative damage and aversivememory in a 6-OHDA model of Parkinson's disease. Arq Neuropsiquiatr 2016; 74: 723-29.##Ren B, Yuan T, Zhang X, Wang L, Pan J, Liu Y, et al. Protective effects of sesamol on systemic inflammation and cognitive impairment in aging mice. J Agric Food Chem 2020; 68: 3099-111.##Schapira AH. The clinical relevance of levodopa toxicity in the treatment of Parkinson's disease. Mov Disord 2008; 23: S515-S20.##Schwarting R, Huston J. Behavioral and neurochemical dynamics of neurotoxic meso-striatal dopamine lesions. Neurotoxicology 1997; 18: 689-708. S##hahidani S, Rajaei Z, Alaei H. Pretreatment with crocin along with treadmill exercise ameliorates motor and memory deficits in hemiparkinsonian rats by anti-inflammatory and antioxidant mechanisms. Metab Brain Dis 2019; 34: 459-68.##hi K, Liu X, Hou L, Qiao D, Lin X. Effects of exercise on mGluR-mediated glutamatergic transmission in the striatum of hemiparkinsonian rats. Neurosci Lett 2019; 705: 143-50.##Shulman JM, De Jager PL, Feany MB. Parkinson's disease: genetics and pathogenesis. Ann Rev Pathol 2011; 6: 193-222.##Sonia Angeline M, Sarkar A, Anand K, Ambasta RK, Kumar P. Sesamol and naringenin reverse the effect of rotenone-induced PD rat model. Neuroscience 2013; 254: 379-94.##Speck AE, Schamne MG, S Aguiar A Jr, Cunha RA, Prediger RD. Treadmill exercise attenuates L-DOPA-induced dyskinesia and increases striatal levels of glial cell-derived neurotrophic factor (GDNF) in hemiparkinsonian mice. Mol Neurobiol 2019; 56: 2944-51.##Subramaniam SR, Chesselet MF. Mitochondrial dysfunction and oxidative stress in Parkinson's disease. Prog Neurobiol 2013; 106: 17-32.##Sung YH. Effects of treadmill exercise on hippocampal neurogenesis in an MPTP/probenecidinduced Parkinson's disease mouse model. J Phys Ther Sci 2015; 27: 3203-6.##Tajiri N, Yasuhara T, ShingoT, Kondo A, Yuan W, Kadota T, et al. Exercise exerts neuroprotective effects on Parkinson's disease model of rats. Brain Res 2010; 1310: 200-7.##Tuon T, Souza PS, Santos MF, Pereira FT, Pedroso GS, Luciano TF, et al. Physical training regulates mitochondrial parameters and neuroinflammatory mechanisms in an experimental model of Parkinson's disease. Oxid Med Cell Longev 2015; 2015.##Um HS, Kang EB, Leem YH, Cho IH, Yang CH, Chae KR, et al. Exercise training acts as a therapeutic strategy forreduction of the pathogenic phenotypes for Alzheimer's disease in an NSE/APPsw-transgenic model. Int J Mol Med 2008; 22: 529-39.##Zaman V, Shields DC, Shams R, Drasites KP, Matzelle D, Haque A, et al. Cellular and molecular pathophysiology in the progression of Parkinson's disease. Metab Brain Dis 2021.##Zhang P, Wang Y, Wang H, Cao J. Sesamol alleviates chronic intermittent hypoxia-induced cognitive deficits via inhibiting oxidative stress and inflammation in rats. Neuroreport 2021; 32: 105-11.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The protective effects of escitalopram on chronic restraint stress-induced memory deficits in adult rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Stress influences brain functions adversely but escitalopram exhibits positive effects on cognitive processes. Therefore, this study investigated the protective effects of different escitalopram doses on cognitive functions in rats under chronic stress and normal conditions. Methods: Forty-nine rats were randomly allocated into seven groups: control, sham, stress, escitalopram (10, 20 mg/kg/day) and stress-escitalopram (both doses). Initial latency, latency after 1-day, dark stay (DS) time and the number of entrances to the dark compartment were evaluated by passive avoidance test. Results: There were significant latency differences in stress and escitalopram10 groups compared to control group. Additionally, latencies showed significant enhancements in both 10 and 20 mg/kg/day stress-escitalopram groups compared to stress group and significant decrease in escitalopram20 group with respect to escitalopram10 group. DS time was significantly higher in stressed group and significantly lower in escitalopram10 groups, both compared to control group. Also, it was significantly lower in both stress-escitalopram groups in comparison with stress group. Furthermore, escitalopram20 group had a significantly higher DS time compared to escitalopram10 group. Finally, the number of entrances to the dark compartment was significantly lower in stress, escitalopram10 and stress-escitalopram10 groups compared to control group. Conclusion: Different doses of escitalopram affected brain functions under chronic stress and normal conditions. Escitalopram10 presented the most beneficial effects on improving brain functions under normal conditions. Whereas, both escitalopram doses showed similar protective effects on memory under stress. Overall, escitalopram at a dose of 10 mg/kg/day improved learning, memory consolidation and locomotor activity better than its maximum dose of 20 mg/kg/day.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>39</FPAGE>
			<TPAGE>48</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/8
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/9/18
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/12
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/23
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Zahra</Name>
				<MidName></MidName>
				<Family>Farahbakhsh</Family>
				<NameE>Zahra</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Farahbakhsh</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maryam</Name>
				<MidName></MidName>
				<Family>Radahmadi</Family>
				<NameE>Maryam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Radahmadi</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>m_radahmadi@med.mui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Escitalopram</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Stress</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Learning</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Memory</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Passive avoidance.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
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Biol Psychiatry 2014; 76: 223-30.##Diamond DM, Campbell AM, Park CR, Woodson JC, Conrad CD, Bachstetter AD, et al. Influence of predator stress on the consolidation versus retrieval of long-term spatial memory and hippocampal spinogenesis. Hippocampus 2006; 16: 571-6.##Do Couto FS, Batalha VL, Valadas JS, Data-Franca J, Ribeiro JA, Lopes LV. Escitalopram improves memory deficits induced by maternal separation in the rat. Eur J Pharmacol 2012; 695: 71-5.##Do Nascimento EB, Dierschnabel AL, de Macêdo Medeiros A, Suchecki D, Silva RH, Ribeiro AM. Memory impairment induced by different types of prolonged stress is dependent on the phase of the estrous cycle in female rats. Horm Behav 2019; 115: 104563.##Drozd R, Rychlik M, Fijalkowska A, Rygula R. Effects of cognitive judgement bias and acute antidepressant treatment on sensitivity to feedback and cognitive flexibility in the rat version of the probabilistic reversal-learning test. Behav Brain Res 2019; 359: 619-29.##Duque A, Vinader-Caerols C, Monleón S. Effects of social stress and clomipramine on emotional memory in mice. A Acta Neurobiol Exp (Wars) 2016; 76: 225-33.##Gammoh O, Mayyas F, Darwish Elhajji F. Chlorpheniramine and escitalopram: Similar antidepressant and nitric oxide lowering roles in a mouse model of anxiety. Biomed Rep 2017; 6: 675-80.##Ghadrdoost B, Vafaei AA, Rashidy-Pour A, Hajisoltani R, Bandegi AR, Motamedi F, et al. Protective effects of saffron extract and its active constituent crocin against oxidative stress and spatial learning and memory deficits induced by chronic stress in rats. Eur J Pharmacol 2011; 667: 222-9.##Hadad-Ophir O, Albrecht A, Stork O, Richter-Levin G. Amygdala activation and gabaergic gene expression in hippocampal sub-regions at the interplay of stress and spatial learning. Front Behav Neurosci 2014; 8: 3.##Ibrahim WW, Abdelkader NF, Ismail HM, Khattab MM. 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The antidepressant- and anxiolytic-like effects following co-treatment with escitalopram and risperidone in rats. J Physiol Pharmacol 2016; 67: 471-80.##Kirino E. Antidepressant efficacy of escitalopram in major depressive disorder; in: Melatonin, neuroprotective agents and antidepressant therapy. 2016; p. 465-76.##Li XL, Yuan YG, Xu H, Wu D, Gong WG, Geng LY, et al. Changed synaptic plasticity in neural circuits of depressive-like and escitalopram-treated rats. Int J Neuropsychopharmacol 2015; 18.##Lim LW, Blokland A, Tan S, Vlamings R, Sesia T, Aziz-Mohammadi M, et al. Attenuation of fear-like response by escitalopram treatment after electrical stimulation of the midbrain dorsolateral periaqueductal gray. Exp Neurol 2010; 226: 293-300.##Lin CC, Tung CS, Liu YP. Escitalopram reversed the traumatic stress-induced depressed and anxiety-like symptoms but not the deficits of fear memory. Psychopharmacology 2016; 233: 1135-46.##Ma L, Lu ZN, Hu P, Yao CJ. 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Arch Physiol Biochem 2019; 125: 293-301.##Mowla A, Mosavinasab M, Haghshenas H, Borhani Haghighi A. Does serotonin augmentation have any effect on cognition and activities of daily living in alzheimer's dementia? A doubleblind, placebo-controlled clinical trial. J Clin Psychopharmacol 2007; 27: 484-7.##Msetfi RM, Kumar P, Harmer CJ, Murphy RA. Ssri enhances sensitivity to background outcomes and modulates response rates: A randomized double blind study of instrumental action and depression. Neurobiol Learn Mem 2016; 131: 76-82.##Murdoch D, Keam SJ. Escitalopram. Drugs 2005; 65: 2379-404.##Patchev VK, Patchev AV. Experimental models of stress. Dialogues Clin Neurosci 2006; 8: 417-32.##Patki G, Solanki N, Atrooz F, Allam F, Salim S. Depression, anxiety-like behavior and memory impairment are associated with increased oxidative stress and inflammation in a rat model of social stress. Brain Res 2013; 1539: 73-86.##Pechlivanova DM, Stoynev AG, Tchekalarova JD. The effects of chronic losartan pretreatment on restraint stress-induced changes in motor activity, nociception and pentylenetetrazol generalized seizures in rats. Folia Med (Plovdiv) 2011; 53: 69-73.##Radahmadi M, Alaei H, Sharifi MR, Hosseini N. Effects of different timing of stress on corticosterone, BDNF and memory in male rats. Physiol Behav 2015; 139: 459-67.##Radahmadi M, Hosseini N, Alaei H, Sharifi MR. Effects of stress on serum and hippocampal il1β and glucose levels as well as retention in rats. Indian J Physiol Pharmacol 2017; 61: 141-51.##Ranjbar H, Radahmadi M, Alaei H, Reisi P, Karimi S. The effect of basolateral amygdala nucleus lesion on memory under acute,mid and chronic stress in male rats. Turk J Med Sci 2016; 46: 1915-25.##Ren QG, Wang YJ, Gong WG, Xu L, Zhang ZJ. Escitalopram ameliorates tau hyperphosphorylation and spatial memory deficits induced by protein kinase a activation in sprague dawley rats. J Alzheimers Dis 2015; 47: 61-71.##Riga MS, Sanchez C, Celada P, Artigas F. Sub-chronic vortioxetine (but not escitalopram) normalizes brain rhythm alterations and memory deficits induced by serotonin depletion in rats. Neuropharmacology 2020; 178: 108238.##Rose EJ, Simonotto E, Spencer EP, Ebmeier KP. The effects of escitalopram on working memory and brain activity in healthy adults during performance of the n-back task. Psychopharmacology (Berl) 2006; 185: 339-47.##Sánchez C, Gruca P, Bien E, Papp M. R-citalopram counteracts the effect of escitalopram in a rat conditioned fear stress model of anxiety. Pharmacol Biochem Behav. 2003; 75: 903-7.##Sardari M, Rezayof A, Zarrindast MR. 5-ht1a receptor blockade targeting the basolateral amygdala improved stress-induced impairment of memory consolidation and retrieval in rats. Neuroscience 2015; 300: 609-18.##Schilström B, Konradsson-Geuken A, Ivanov V, Gertow J, Feltmann K, Marcus MM, et al. Effects of s-citalopram, citalopram, and r-citalopram on the firing patterns of dopamine neurons in the ventral tegmental area, n-methyl-d-aspartate receptor-mediated transmission in the medial prefrontal cortex and cognitive function in the rat. Synapse (New York, NY) 2011; 65: 357-67.##Schöner J, Heinz A, Endres M, Gertz K, Kronenberg G. Post-traumatic stress disorder and beyond: An overview of rodent stress models. J Cell Mol Med 2017; 21: 2248-56.##Seo MK, Lee JG, Park SW. Effects of escitalopram and ibuprofen on a depression-like phenotype induced by chronic stress in rats. Neurosci Lett 2019; 696: 168-73.##Shabani M, Divsalar K, Janahmadi M. Destructive effects of prenatal win 55212-2 exposure on central nervous system of neonatal rats. Addict Health 2012; 4: 9-19.##Shetty S, Hariharan A, Shirole T, Jagtap AG: Neuroprotective potential of escitalopram against behavioral, mitochondrial and oxidative dysfunction induced by 3-nitropropionic acid. 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Indian J Pharmacol 2000; 32: 242-5.##Wang YJ, Ren QG, Gong WG, Wu D, Tang X, Li XL, et al. Escitalopram attenuates β-amyloidinduced tau hyperphosphorylation in primary hippocampal neurons through the 5-ht1a receptor mediated akt/gsk-3β pathway. Oncotarget 2016; 7: 13328-39.##Waugh J, Goa KL. Escitalopram. A review of its use in the management of major depressive and anxiety disorders. CNS Drugs 2003; 17: 343-62.##Wood GE, Young LT, Reagan LP, McEwen BS. Acute and chronic restraint stress alter the incidence of social conflict in male rats. Horm Behav. 2003; 43: 205-13.##Wu C, Gong WG, Wang YJ, Sun JJ, Zhou H, Zhang ZJ, et al. Escitalopram alleviates stressinduced alzheimer's disease-like tau pathologies and cognitive deficits by reducing hypothalamic-pituitary-adrenal axis reactivity and insulin/gsk-3β signal pathway activity. Neurobiol Aging 2018; 67: 137-47.##Xi G, Hui J, Zhang Z, Liu S, Zhang X, Teng G, et al. Learning and memory alterations are associated with hippocampal n-acetylaspartate in a rat model of depression as measured by 1hmrs. PloS One 2011; 6: 28686.##Yang SN, Wang YH, Tung CS, Ko CY, Liu YP. Effects of escitalopram on a rat model of persistent stress-altered hedonic activities: Towards a new understanding of stress and depression. Chin J Physiol 2015; 58: 404-11.##Zoladz PR, Park CR, Halonen JD, Salim S, Alzoubi KH, Srivareerat M, et al. Differential expression of molecular markers of synaptic plasticity in the hippocampus, prefrontal cortex, and amygdala in response to spatial learning, predator exposure, and stress-induced amnesia. Hippocampus 2012; 22: 577-89.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Evaluating the impact of Viola spathulata in a rat model of brain ischemia/reperfusion by influencing expression level of caspase-3 and cyclooxygenase-2</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Focal cerebral ischemia followed by reperfusion causes ischemia/reperfusion (I/R) brain injury. I/R injury is a complex pathophysiological process involving inflammation and apoptosis in neurons. Previous studies reported the anti-inflammatory traits of the family Violaceae. We aimed to evaluate the effects of Viola spathulata pre-treatment on infarct volume (IV), neurological deficit score (NDS) and alterations in mRNA level of cyclooxygenase 2 (COX2) and caspase 3 (CASP3) in a rat middle cerebral artery occlusion (MCAO) model. Methods: Thirty-three male Wistar rats were randomly distributed in 4 groups: normal control, MCAO control, MCAO + 5 mg/kg V. spathulata and MCAO + 10 mg/kg V. spathulata. Two doses of V. spathulata extracts were injected intraperitoneally for 7 days before the onset of ischemia. Finally, IV, NDS and mRNA expression of CASP3 and COX2 genes were assessed 24h after reperfusion. Results: IV and NDS in MCAO rats were remarkably higher compared with normal control rats and pre-treatment with V. spathulata extracts markedly reduced IV and NDS in the core, penumbra and subcortical regions of MCAO rats. Also, the level of COX2 and CASP3 mRNA was higher in the MCAO control group relative to normal control. Pre-treatment with V. spathulata extracts markedly reduced CASP3 mRNA relative to MCAO rats. Conclusion: It was found that V. spathulata might reduce ischemic damage in the brain of MCAO rats partly by decreasing apoptotic effects of CASP3. Further research is recommended to investigate signaling pathways involved in apoptosis.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>49</FPAGE>
			<TPAGE>59</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/14
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/7/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mahsa</Name>
				<MidName></MidName>
				<Family>Ramezanpour</Family>
				<NameE>Mahsa</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ramezanpour</FamilyE>
				<Organizations>
				<Organization>Medical Biotechnology Research Center, School of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Korosh</Name>
				<MidName></MidName>
				<Family>Khanaki</Family>
				<NameE>Korosh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khanaki</FamilyE>
				<Organizations>
				<Organization>Medical Biotechnology Research Center, School of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Masomeh</Name>
				<MidName></MidName>
				<Family>Faezi</Family>
				<NameE>Masomeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Faezi</FamilyE>
				<Organizations>
				<Organization>Department of Medical Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ekram</Name>
				<MidName></MidName>
				<Family>Mohammadi</Family>
				<NameE>Ekram</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mohammadi</FamilyE>
				<Organizations>
				<Organization>Department of Medical Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Abbas</Name>
				<MidName></MidName>
				<Family>Gholipour</Family>
				<NameE>Abbas</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Gholipour</FamilyE>
				<Organizations>
				<Organization>Department of Biology, School of Sciences, Payame Noor University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahmood</Name>
				<MidName></MidName>
				<Family>Abedinzade</Family>
				<NameE>Mahmood</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Abedinzade</FamilyE>
				<Organizations>
				<Organization>Medical Biotechnology Research Center, School of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>mabedinzade@gums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Ischemia</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Reperfusion</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Viola spathulata</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Caspase 3 (CASP3)</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Cyclooxygenase 2 (COX2)</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Abedinzadeh M, Mohammadi E, Hedayati M, Nikokar I, Bostani Z. Protective effect of the viola spathulata extract on NCX3 gene expression in an animal model of cerebral ischemia. Basic Clin Neurosci 2021.##Ansari M, Rafiee K, Yasa N, Vardasbi S, Naimi S, Nowrouzi A. Measurement of melatonin in alcoholic and hot water extracts of Tanacetum parthenium, Tripleurospermum disciforme and Viola odorata. Daru 2010; 18: 173-8.##Asahi M, Hoshimaru M, Uemura Y, Tokime T, Kojima M, Ohtsuka T, et al. Expression of interleukin-1β converting enzyme gene family and bcl-2 gene family in the rat brain following permanent occlusion of the middle cerebral artery. J Cereb Blood Flow Metab 1997; 17: 11-18.##Bai S, Hu Z, Yang Y, Yin Y, Li W, Wu L, et al. Anti‐Inflammatory and Neuroprotective Effects of Triptolide via the NF‐κ B Signaling Pathway in a Rat MCAO Model. Anatomical Record 2016; 299: 256-66.##Bansal S, Sangha KS, Khatri P. Drug treatment of acute ischemic stroke. Am J Cardiovasc Drugs 2013; 13: 57-69.##Chan PH. Reactive oxygen radicals in signaling and damage in the ischemic brain. J Cereb Blood Flow Metab 2001; 21: 2-14.##Chen YF, Wang YW, Huang WS, Lee MM, Wood WG, Leung YM, et al. Transcinnamaldehyde, an essential oil in cinnamon powder, ameliorates cerebral ischemia-induced brain injury via inhibition of neuroinflammation through attenuation of iNOS, COX-2 expression and NFκ-B signaling pathway. Neuromolecular Med 2016; 18: 322-33.##Daemen MA, van't Veer C, Denecker G, Heemskerk VH, Wolfs TG, Clauss M, et al. Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation. J Clin Invest 1999; 104: 541-9.##Endres M, Namura S, Shimizu-Sasamata M, Waeber C, Zhang L, Gómez-Isla T, et al. Attenuation of delayed neuronal death after mild focal ischemia in mice by inhibition of the caspase family. J Cereb Blood Flow Metab 1998; 18: 238-47.##Erfani S, Moghimi A, Aboutaleb N, Khaksari M. Nesfatin-1 improve spatial memory impairment following transient global cerebral ischemia/reperfusion via inhibiting microglial and caspase-3 activation. J Mol Neurosci 2018; 65: 377-84.##Gao L, Ji X, Song J, Liu P, Yan F, Gong W, et al. Puerarin protects against ischemic brain injury in a rat model of transient focal ischemia. Neurol Res 2009; 31: 402-6.##Gu J, Su S, Guo J, Zhu Y, Zhao M, Duan JA. Anti‐inflammatory and anti‐apoptotic effects of the combination of Ligusticum chuanxiong and Radix Paeoniae against focal cerebral ischaemia via TLR 4/MyD88/MAPK/NF‐κB signalling pathway in MCAO rats. J Pharm Pharmacol 2018; 70: 268-77.##Gu Y, Chen J, Shen J. Herbal medicines for ischemic stroke: combating inflammation as therapeutic targets. J Neuroimmune Pharmacol 2014; 9: 313-39.##Ha S K, Lee P, Park J A, Oh H R, Lee S Y, Park JH, et al. Apigenin inhibits the production of NO and PGE2 in microglia and inhibits neuronal cell death in a middle cerebral artery occlusion-induced focal ischemia mice model. Neurochem Int 2008; 52: 878-86.##Haylor JL, Harris KP, Nicholson ML, Waller HL, Huang Q, Yang B. Atorvastatin improving renal ischemia reperfusion injury via direct inhibition of active caspase-3 in rats. Exp Biol Med 2011; 236: 755-63.##Iadecola C, Alexander M. Cerebral ischemia and inflammation. Curr Opin Neurol 2001; 14: 89-94.##Johnson CO, Nguyen M, Roth GA, Nichols E, Alam T, Abate D, et al. Global, regional, and national burden of stroke, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol 2019; 18: 439-58.##Khanaki K, Abedinzade M, Hamidi M. The effects of urtica dioica and lamium album extracts on the expression level of cyclooxygenase-2 and caspase-3 in the liver and kidney of streptozotocin-induced diabetic rats. Pharm Sci 2019; 25: 37-43.##Kim YJ, Yoon YH, Park WJ. Supply of tryptophan and tryptamine influenced the formation of melatonin in Viola plants. J Life Sci 2011; 21: 328-33.##Kuroda S, Siesjö B. Reperfusion damage following focal ischemia: pathophysiology and therapeutic windows. Clinical Neuroscience 1997; 4: 199-212.##Lee KM, Kang BS, Lee HL, Son SJ, Hwang SH, Kim DS, et al. Spinal NF‐kB activation induces COX‐2 upregulation and contributes to inflammatory pain hypersensitivity. Eur J Neurosci 2004; 19: 3375-81.##Lee MY, Yuk JE, Kwon OK, Kim HS, Oh SR, Lee HK, et al. Anti-inflammatory and antiasthmatic effects of Viola mandshurica W. Becker (VM) ethanolic (EtOH) extract on airway inflammation in a mouse model of allergic asthma. J Ethnopharmacol 2010; 127: 159-64.##Lei B, Popp S, Capuano-Waters C, Cottrell J, Kass I. Lidocaine attenuates apoptosis in the ischemic penumbra and reduces infarct size after transient focal cerebral ischemia in rats. Neuroscience 2004; 125: 691-701.##Letechipıá -Vallejo G, González-Burgos I, Cervantes M. Neuroprotective effect of melatonin on brain damage induced by acute global cerebral ischemia in cats. Arch Med Res 2001; 32: 186-92.##Li Z, Hua C, Pan X, Fu X, Wu W. Carvacrol exerts neuroprotective effects via suppression of the inflammatory response in middle cerebral artery occlusion rats. Inflammation 2016; 39: 1566-72.##Liu L, Qin Q, Qian Z, Shi M, Deng Q, Zhu W, et al. Protective effects of melatonin on ischemia-reperfusion induced myocardial damage and hemodynamic recovery in rats. Eur Rev Med Pharmacol Sci 2014; 18: 3681-86.##Longa EZ, Weinstein PR, Carlson S, Cummins R. Reversible middle cerebral artery occlusion without craniectomy in rats. stroke 1989; 20: 84-91.##Lucas SM, Rothwell NJ, Gibson RM. The role of inflammation in CNS injury and disease. Br J Pharmacol 2006; 147: 232-40.##Moliner C, Barros L, Dias MI, Reigada I, Ferreira IC, López V, et al. Viola cornuta and Viola x wittrockiana: Phenolic compounds, antioxidant and neuroprotective activities on Caenorhabditis elegans. J Food Drug Anal 2019; 27: 849-59.##Mousavi SH, Naghizade B, Pourgonabadi S, Ghorbani A. Protective effect of Viola tricolor and Viola odorata extracts on serum/glucose deprivation-induced neurotoxicity: role of reactive oxygen species. Avicenna J Phytomed 2016; 6: 434-41.##Muhammad N, Saeed M, Khan H. Antipyretic, analgesic and anti-inflammatory activity of Viola betonicifolia whole plant. BMC Complement Altern Med 2012; 12: 59.##Park S, Nam K, Lee H, Cho E, Koo U, Mar W. Neuroprotective effects of an alkaloid-free ethyl acetate extract from the root of Sophora flavescens Ait. against focal cerebral ischemia in rats. Phytomedicine 2009; 16: 1042-51.##Pasbakhsh P, Saeednia S, Abolhassani F, Khansari G, Sobhani A. Melatonin prevents ischemia-reperfusion injury following superior mesenteric artery occlusion in the rat. Daru 2008; 16: 95-101.##Petrovic-Djergovic D, Goonewardena SN, Pinsky DJ. Inflammatory disequilibrium in stroke. Circ Res 2016; 119: 142-58.##asouli Vani J, Taghi Mohammadi M, Sarami Foroshani M, Rezazade E. Evaluation of the neuroprotective and antioxidant effects of Dorema aucheri extract on cerebral ischaemiareperfusion injury in rats. Pharm Biol 2019; 57: 255-62.##Robertson NJ, Faulkner S, Fleiss B, Bainbridge A, Andorka C, Price D, et al. Melatonin augments hypothermic neuroprotection in a perinatal asphyxia model. Brain 2013; 136: 90- 105.##Sanderson TH, Reynolds CA, Kumar R, Przyklenk K, Hüttemann M. Molecular mechanisms of ischemia-reperfusion injury in brain: pivotal role of the mitochondrial membrane potential in reactive oxygen species generation. Mol Neurobiol 2013; 47: 9-23.##Singh D, Hembrom S. Neuroprotective effect of flavonoids: A systematic review. Int J Aging Res 2019; 2: 26.##Svangård E, Göransson U, Hocaoglu Z, Gullbo J, Larsson R, Claeson P, et al. Cytotoxic Cyclotides from Viola t ricolor. J Nat Prod 2004; 67: 144-47.##Swanson RA, Morton MT, Tsao-Wu G, Savalos RA, Davidson C, Sharp FR. A semiautomated method for measuring brain infarct volume. J Cereb Blood Flow Metab 1990; 10: 290-3.##Tan DX, Zheng X, Kong J, Manchester LC, Hardeland R, Kim SJ, et al. Fundamental issues related to the origin of melatonin and melatonin isomers during evolution: relation to their biological functions. Int J Mol Sci 2014; 15: 15858-90.##Tayarani-Najaran Z, Yazdian-Robati R, Amini E, Salek F, Arasteh F, Emami SA. The mechanism of neuroprotective effect of Viola odorata against serum/glucose deprivationinduced PC12 cell death. Avicenna J Phytomedicine 2019; 9: 491-8.##Vukics V, Kery A, Bonn GK, Guttman A. Major flavonoid components of heartsease (Viola tricolor L.) and their antioxidant activities. Anal Bioanal Chem 2008; 390: 1917-25.##Youdim KA, Dobbie MS, Kuhnle G, Proteggente AR, Abbott NJ, Rice‐Evans C. Interaction between flavonoids and the blood-brain barrier: in vitro studies. J Neurochem 2003; 85: 180- 92.##Zhu H, Qin SS, Zhang N, Yang DW, Han HR, Wei KH, et al. Chemical constituents and biological activities of plants from the Genus Viola. Chem Biodivers 2015; 12: 1777-808.##Zhu N, Li H, Han M, Guo L, Chen L, Yun Y, et al. Environmental nitrogen dioxide (NO2) exposure influences development and progression of ischemic stroke. Toxicol Lett 2012; 214: 120-30.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The interactive effect of berberine chloride and exercise rehabilitation on the lung tissue apoptosis and oxidative stress biomarkers in rats exposed to diazinon</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: A serious complication of diazinon is the occurrence of oxidative stress in the respiratory system. The combination of medication and exercise rehabilitation has not been studied. The aim of this study was to assess the effects of berberine chloride alongside resistance training on apoptosis and oxidative stress markers of lung tissue in male rats exposed to diazinon. Methods: Forty-eight adult male Wistar rats were divided into 1: resistance exercise + berberine
chloride dose 2mg/kg + diazinon; 2: resistance exercise + berberine chloride dose 15mg/kg + diazinon; 3: toxic (diazinon 1.5 mg/kg); 4: resistance training + diazinon; 5: berberine chloride dose 2mg/kg + diazinon; 6: berberine chloride dose 15mg/kg + diazinon; 7: intact control and 8: normal saline. To induce oxidative stress, diazinon was injected intraperitoneally 1.5mg/kg. Berberine chloride was used as 2 and 15mg/kg through intraperitoneal injection for 4 weeks. Resistance training was conducted 3 sessions/week for 4 weeks including climbing a vertical ladder. Lung tissue was exposed to evaluate pathohistological test, apoptosis and oxidative stress markers. Results: Berberine chloride and exercise had a significant effect on decreasing ROS, MDA, caspase-3, and increasing GSH level, but no effect on the 8-OHDG. The exercise alone has no significant effect on ROS, MDA, 8-OHDG, caspase-3 and GSH. Conclusion: Berberine chloride alongside sport rehabilitation should be used as an effective treatment on lung apoptosis and oxidative stress with acute poisoning of diazinon. The most important mechanism is the effect of improving oxidative defense and anti-inflammatory effects.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>60</FPAGE>
			<TPAGE>69</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/18
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/5/28
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Reza</Name>
				<MidName></MidName>
				<Family>Niazi</Family>
				<NameE>Reza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Niazi</FamilyE>
				<Organizations>
				<Organization>Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maghsoud</Name>
				<MidName></MidName>
				<Family>Peeri</Family>
				<NameE>Maghsoud</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Peeri</FamilyE>
				<Organizations>
				<Organization>Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>m.peeri@iauctb.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad Ali</Name>
				<MidName></MidName>
				<Family>Azarbayjani</Family>
				<NameE>Mohammad Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Azarbayjani</FamilyE>
				<Organizations>
				<Organization>Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Berberine chloride</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Sport medicine</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Apoptosis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Oxidative stress</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Diazinon.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Al-Attar A M, Al-Taisan W. Preventive effects of black seed (Nigella sativa) extract on Sprague Dawley rats exposed to diazinon. Aust J Basic Appl Sci 2010; 4: 957-68.##Ayala A, Munoz M F, Arguelles S. Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal. Oxid Med Cell Longev 2014; 2014: 360438.##Bas H, Kalender Y. Chlorpyrifos induced cardiotoxicity in rats and the protective role of quercetin and catechin. Gazi Univ J Sci 2011; 24: 387-95.##Ciolac EG, Guimarães VG. Physical exercise and metabolic syndrome. Rev Bras Med Esporte 2004; 10: 319-24.##Close GL, Ashton T, Cable T, Doran D, Holloway C, McArdle F, et al. Ascorbic acid supplementation does not attenuate post-exercise muscle soreness following muscle-damaging exercise but may delay the recovery process. Br J Nutr 2006; 95: 976-81.##de Lemos ET, Oliveira J, Pinheiro JP, Reis F. Regular physical exercise as a strategy to improve antioxidant and anti-inflammatory status: benefits in type 2 diabetes mellitus. Oxid Med Cell Longev 2012; 2012: 741545.##Dinham B. Prolonged exposure to some agricultural pesticides may increase the risk of lung cancer in agricultural workers. Int J Evid Based Healthc 2005; 9: 203-5.##Dressel TD, Goodale Jr R, Zweber B, Borner JW. The effect of atropine and duct decompression on the evolution of Diazinon-induced acute canine pancreatitis. Ann Surg 1982; 195: 424-34.##Apoptosis: a review of programmed cell death. Toxicol Pathol 2007; 35: 495-516.##Gallo M, Lawryk N. Organic phosphorus pesticides. dalam WJ Hayes, Jr. &#38; ER Laws, Jr.(ed.). Handbook of pesticide toxicology. Classes of pesticides Journal 1991.##Gleeson M, Bishop NC, Stensel DJ, Lindley MR, Mastana SS, Nimmo MA. The antiinflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease. Nat Rev Immunol 2011; 11: 607-15.##Heidarvand L, Maali-Amiri R. Physio-biochemical and proteome analysis of chickpea in early phases of cold stress. J Plant Physio 2013; 170: 459-69.##Hosseinzadeh H, Ramezani M, Shafaei H, Taghiabadi E. Anticonvulsant effect of Berberis integerrima L. root extracts in mice. J Acupunct Meridian Stud 2013; 6: 12-17.##Kabasakalis A, Nikolaidis S, Tsalis G, Christoulas K, Mougios V. Effects of sprint interval exercise dose and sex on circulating irisin and redox status markers in adolescent swimmers. J Sports Sci 2019; 37: 827-32.##Kabasakalis A, Tsalis G, Zafrana E, Loupos D, Mougios V. Effects of endurance and highintensity swimming exercise on the redox status of adolescent male and female swimmers. J Sports Sci 2014; 32: 747-56.##Kalender S, Ogutcu A, Uzunhisarcikli M, Açikgoz F, Durak D, Ulusoy Y, et al. Diazinoninduced hepatotoxicity and protective effect of vitamin E on some biochemical indices and ultrastructural changes. Toxicology 2005; 211: 197-206.##Kong W, Wei J, Abidi P, Lin M, Inaba S, Li C, et al. Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins. Nat Med 2004; 10: 1344-51.##Kuepper T, Morrison A, Gieseler U, Schoeffl V. Sport climbing with pre-existing cardiopulmonary medical conditions. International journal of sports medicine 2009; 30: 395-402.##Kuo CL, Chi CW, Liu TY. The anti-inflammatory potential of berberine in vitro and in vivo. Cancer Lett 2004; 203: 127-37.##Lamkhioued B, Renzi PM, Abi-Younes S, Garcia-Zepada EA, Allakhverdi Z, Ghaffar O, et al. Increased expression of eotaxin in bronchoalveolar lavage and airways of asthmatics contributes to the chemotaxis of eosinophils to the site of inflammation. J Immunol 1997; 159: 4593-601.##Lee CH, Chen JC, Hsiang CY, Wu SL, Wu HC, Ho TY. Berberine suppresses inflammatory agents-induced interleukin-1beta and tumor necrosis factor-alpha productions via the inhibition of IkappaB degradation in human lung cells. Pharmacol Res 2007; 56: 193-201.##Li X D, Sun GF, Zhu WB, Wang YH. Effects of high intensity exhaustive exercise on SOD, MDA, and NO levels in rats with knee osteoarthritis. Genet Mol Res 2015; 14: 12367-76.##Lohar DP, Haridas S, Gantt JS, VandenBosch KA. A transient decrease in reactive oxygen species in roots leads to root hair deformation in the legume-rhizobia symbiosis. New Phytol 2007; 173: 39-49.##Mantena SK, Sharma SD, Katiyar SK. Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells. Mol Cancer Ther 2006; 5: 296-308.##Memisogullari R, Taysi S, Bakan E, Capoglu I. Antioxidant status and lipid peroxidation in type II diabetes mellitus. Cell Biochem Funct 2003; 21: 291-6.##Miron VV, Bottari NB, Assmann CE, Stefanello N, da Costa P, Pelinson LP, et al. Physical exercise prevents alterations in purinergic system and oxidative status in lipopolysaccharideinduced sepsis in rats. J Cell Biochem 2019; 120: 3232-42.##Park SK, Larson JL. The relationship between physical activity and metabolic syndrome in people with chronic obstructive pulmonary disease. J Cardiovasc Nurs 2014; 29: 499-507.##Patwardhan B. Ayurveda and future drug development. J Altern Complement Med 1992; 19: 9- 10.##Poet TS, Wu H, Kousba AA, Timchalk C. In vitro rat hepatic and intestinal metabolism of the organophosphate pesticides chlorpyrifos and diazinon. Toxicol Sci 2003; 72: 193-200.##Radak Z, Zhao Z, Koltai E, Ohno H, Atalay M. Oxygen consumption and usage during physical exercise: the balance between oxidative stress and ROS-dependent adaptive signaling. Antioxid Redox Signal 2013; 18: 1208-46.##Sahin I, Onbasi K, Sahin H, Karakaya C, Ustun Y, Noyan T. The prevalence of pancreatitis in organophosphate poisonings. Hum Exp Toxicol 2002; 21: 175-7.##Sekhar RV, McKay SV, Patel SG, Guthikonda AP, Reddy VT, Balasubramanyam A, et al. Glutathione synthesis is diminished in patients with uncontrolled diabetes and restored by dietary supplementation with cysteine and glycine. Diabetes Care 2011; 34: 162-7.##Storm JE, Rozman KK, Doull J. Occupational exposure limits for 30 organophosphate pesticides based on inhibition of red blood cell acetylcholinesterase. Toxicology 2000; 150: 1-29.##Valavanidis A, Vlachogianni T, Fiotakis C. 8-hydroxy-2' -deoxyguanosine (8-OHdG): A critical biomarker of oxidative stress and carcinogenesis. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2009; 27: 120-39.##Vuddanda PR, Chakraborty S, Singh S. Berberine: a potential phytochemical with multispectrum therapeutic activities. Expert Opin Investig Drugs 2010; 19: 1297-307.##Weiner P, Berar-Yanay N, Davidovich A, Magadle R, Weiner M. Specific inspiratory muscle training in patients with mild asthma with high consumption of inhaled beta(2)-agonists. Chest 2000; 117: 722-7.##Yoo KY, Hwang IK, Lim BO, Kang TC, Kim DW, Kim SM, et al. Berberry extract reduces neuronal damage and N-Methyl-D-aspartate receptor 1 immunoreactivity in the gerbil hippocampus after transient forebrain ischemia. Biol Pharm Bull 2006; 29: 623-8.##Yue J, Wang Z, Shao D, Chang Z, Hu R, Li L, et al. Cancer cell membrane-modified biodegradable mesoporous silica nanocarriers for berberine therapy of liver cancer. RSC Advances 2018; 8: 40288-97.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Effect of nasal airflow on respiratory pattern variability in rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The nasal airway a common route for normal breathing. Difficulty in nasal breathing due to nasal blockage is associated with abnormal respiratory pattern during sleep. The aim of this study was to investigate whether alteration in nasal airflow can change respiration pattern variability. Methods: Healthy male Wister rats were randomly divided into 4 groups including: control, saline, nasal obstruction and nasal cavity lidocaine anesthesia. The animals underwent bilateral nasal obstruction using cauterization and locally nasal cavity anesthesia using 10% lidocaine. Respiration of conscious animals recorded using whole-body plethysmography. Results: Respiratory signal analysis revealed a dramatic increase in variability of respiratory rhythm that quantified with increase in the standard deviation of inter-breath interval, inspiration time and mean of IBI, expiration and expiration to inspiration time ratio in both nasal obstruction and nasal anesthetized animals. Additionally, Power spectral density analysis showed higher variability in respiratory frequency, which characterized with broader dominant frequency and periodic respiratory pattern in nasal obstruction animals. Conclusion: These results proposed that, nasal airflow influences respiratory pattern variability. Nasal cavity flow receptors may contribute for these observations.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>70</FPAGE>
			<TPAGE>78</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/182020/12/28
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/10/8
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/62021/04/10
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/21
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Saeed</Name>
				<MidName></MidName>
				<Family>Pazhoohan</Family>
				<NameE>Saeed</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Pazhoohan</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>Saeedpazhoohan@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Fatemeh</Name>
				<MidName></MidName>
				<Family>Abbasi Feijani</Family>
				<NameE>Fatemeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Abbasi Feijani</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Farnaz</Name>
				<MidName></MidName>
				<Family>Mehrabbeigi</Family>
				<NameE>Farnaz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mehrabbeigi</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad Reza</Name>
				<MidName></MidName>
				<Family>Palizvan</Family>
				<NameE>Mohammad Reza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Palizvan</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Saeed</Name>
				<MidName></MidName>
				<Family>Hajihashemi</Family>
				<NameE>Saeed</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Hajihashemi</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Nasal obstruction</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Respiratory pattern</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Nasal airflow</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Apnea.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Atkins M, Taskar V, Clayton N, Stone P, Woodcock A. Nasal resistance in obstructive sleep apnea. Chest 1994; 105: 1133-5.##Basner RC, Simon PM, Schwartzstein RM, Weinberger SE, Weiss JW. Breathing route influences upper airway muscle activity in awake normal adults. J Appl Physiol 1989; 66: 1766- 71.##Craig TJ, Teets S, Lehman EB, Chinchilli VM, Zwillich C. Nasal congestion secondary to allergic rhinitis as a cause of sleep disturbance and daytime fatigue and the response to topical nasal corticosteroids. J Allergy Clin Immunol 1998; 101: 633-7.##Douglas NJ, White DP, Weil JV, Zwillich CW. Effect of breathing route on ventilation and ventilatory drive. Respir Physiol 1983; 51: 209-18.##Feldman JL, Del Negro CA, Gray PA. Understanding the rhythm of breathing: so near, yet so far. Annu Rev Physiol 2013; 75: 423-52.##Frey U, Brodbeck T, Majumdar A, Taylor DR, Town GI, Silverman M, et al. Risk of severe asthma episodes predicted from fluctuation analysis of airway function. Nature 2005; 438: 667- 70.##Frey U, Maksym G, Suki B. Temporal complexity in clinical manifestations of lung disease. J Appl Physiol (1985) 2011; 110: 1723-31.##Funaki Y, Hiranuma M, Shibata M, Kokai S, Ono T. Effects of nasal obstruction on maturation of the jaw-opening reflex in growing rats. Arch Oral Biol 2014; 59: 530-8.##Grosmaitre X, Santarelli LC, Tan J, Luo M, Ma M. Dual functions of mammalian olfactory sensory neurons as odor detectors and mechanical sensors. Nat Neurosci 2007; 10: 348-54.##Guilleminault C, Huang YS, Chin WC, Okorie C. The nocturnal-polysomnogram and &#34;nonhypoxic sleep-disordered-breathing&#34; in children. Sleep Med 2019; 60: 31-44.##Harding R, Buttress JA, Caddy DJ, Wood GA. Respiratory and upper airway responses to nasal obstruction in awake lambs and ewes. Respir Physiol 1987; 68: 177-88.##Jubran A, Tobin MJ. Effect of isocapnic hypoxia on variational activity of breathing. Am J Respir Crit Care Med 2000; 162: 1202-9.##Katz ES, Mitchell RB, D'Ambrosio CM. Obstructive sleep apnea in infants. Am J Respir Crit Care Med 2012; 185: 805-16.##Magliulo G, Iannella G, Ciofalo A, Polimeni A, De Vincentiis M, Pasquariello B, et al. Nasal pathologies in patients with obstructive sleep apnoea. Acta Otorhinolaryngol Ital 2019; 39: 250- 6.##McNicholas WT, Coffey M, McDonnell T, O'Regan R, Fitzgerald MX. Upper airway obstruction during sleep in normal subjects after selective topical oropharyngeal anesthesia. Am Rev Respir Dis 1987; 135: 1316-9.##Meen EK, Chandra RK. The role of the nose in sleep-disordered breathing. Am J Rhinol Allergy 2013; 27: 213-20.##Michels Dde S, Rodrigues Ada M, Nakanishi M, Sampaio AL, Venosa AR. Nasal involvement in obstructive sleep apnea syndrome. Int J Otolaryngol 2014; 2014.##Mohammadkarimi N, Jafari M, Mellat A, Kazemi E, Shirali A. Evaluation of efficacy of intranasal lidocaine for headache relief in patients refer to emergency department. J Res Med Sci 2014; 19: 331-5.##Ogawa T, Okihara H, Kokai S, Abe Y, Karin Harumi UK, Makiguchi M, et al. Nasal obstruction during adolescence induces memory/learning impairments associated with BDNF/TrkB signaling pathway hypofunction and high corticosterone levels. J Neurosci Res 2018; 96: 1056- 65.##Parsazadegan T, Salimi M, Ghazvineh S, Raoufy MR. Cognitive disorders in allergic rhinitis may be induced by decline of respiration entrained rhythm in the brain. Med Hypotheses 2018; 121: 89-90.##Patino M, Sadhasivam S, Mahmoud M. Obstructive sleep apnoea in children: perioperative considerations. Br J Anaesth 2013; 111: 83-95.##Peng CK, Mietus JE, Liu Y, Lee C, Hausdorff JM, Stanley HE, et al. Quantifying fractal dynamics of human respiration: age and gender effects. Ann Biomed Eng 2002; 30: 683-92.##Perez W, Tobin MJ. Separation of factors responsible for change in breathing pattern induced by instrumentation. J Appl Physiol (1985) 1985; 59: 1515-20.##Raoufy MR, Ghafari T, Darooei R, Nazari M, Mahdaviani SA, Eslaminejad AR, et al. Classification of Asthma Based on Nonlinear Analysis of Breathing Pattern. PLoS One 2016; 11: e0147976.##Rombaux P, Liistro G, Hamoir M, Bertrand B, Aubert G, Verses T, et al. Nasal obstruction and its impact on sleep-related breathing disorders. Rhinology 2005; 43: 242-50.##Sadeghi A, Pazhoohan S, Hajihashemi S, Palizvan MR, Valizadeh M. Anxiety-like behavior induced by allergen is associated with decreased irregularity of breathing pattern in rats. Respiratory physiology &#38; neurobiology. 2022;298:103847.##Senaratna CV, Perret JL, Lodge CJ, Lowe AJ, Campbell BE, Matheson MC, et al. Prevalence of obstructive sleep apnea in the general population: A systematic review. Sleep Med Rev 2017; 34: 70-81.##Strauss SG, Lynn AM, Bratton SL, Nespeca MK. Ventilatory response to CO2 in children with obstructive sleep apnea from adenotonsillar hypertrophy. Anesth Analg 1999; 89: 328-32.##Suki B, Bates JH, Frey U. Complexity and emergent phenomena. Compr Physiol 2011; 1: 995- 1029.##Tanaka Y, Honda Y. Nasal obstruction as a cause of reduced PCO2 and disordered breathing during sleep. J Appl Physiol (1985) 1989; 67: 970-2.##Thach BT. The Role of the upper airway in SIDS and sudden unexpected infant deaths and the importance of external airway-protective behaviors. In: Duncan JR, Byard RW, editors. SIDS sudden infant and early childhood death: the past, the present and the future. Adelaide (AU): University of Adelaide Press© 2018 The Contributors, with the exception of which is by Federal United States employees and is therefore in the public domain. 2018.##Thamrin C, Frey U. Complexity and respiratory growth: a developing story. J Appl Physiol (1985) 2009; 106: 753-4.##White DP, Cadieux RJ, Lombard RM, Bixler EO, Kales A, Zwillich CW. The effects of nasal anesthesia on breathing during sleep. Am Rev Respir Dis 1985; 132: 972-5.##Yuan H, Pinto SJ, Huang J, McDonough JM, Ward MB, Lee YN, et al. Ventilatory responses to hypercapnia during wakefulness and sleep in obese adolescents with and without obstructive sleep apnea syndrome. Sleep 2012; 35: 1257-67.##Zamoscik VE, Schmidt SL, Gerchen MF, Samsouris C, Timm C, Kuehner C, et al. Respiration pattern variability and related default mode network connectivity are altered in remitted depression. Psychol Med 2018; 48: 2364-74.##Zelano C, Jiang H, Zhou G, Arora N, Schuele S, Rosenow J, et al. Nasal respiration entrains human limbic oscillations and modulates cognitive function. J Neurosci 2016; 36: 12448-67.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Selegiline induces adipose tissue-derived stem cells into neuron-like cells through MAPK signaling pathway</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Adipose-derived stem cells (ADSCs) are one of the most well-known and accessible sources of stem cells that can be used for the treatment of neurodegenerative diseases. On the other hand, previous studies have suggested that selegiline, as an irreversible inhibitor of monoamine oxidase, affects stem cells&#8217; differentiation into neurons. This study was conducted to investigate the involvement in phosphatidylinositol-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways in ADSCs differentiation to neuron-like cells using selegiline as inducer. Methods: ADSCs were isolated from male rats, cultured in DMEM and then treated with selegiline (10-7 M) for 24h. Real-time PCR for nestin and neurofilament-68 (NF-68) was performed from the negative control (ADSCs at the 3rd passage), positive control (ADSCs were treated with 10-7 M selegeline for 24h, PI3AKT inhibitor (ADSCs were pretreated with treated with 10&#181;M LY294002 for 3h, then10-7 M selegeline for the next 24h, and MAPK inhibitor (ADSCs were pretreated with treated with 10&#181;M PD98059 for 3h, then10-7 M selegeline for the next 24h). Results: Nestin and NF-68 genes have been over-expressed in the selegiline-treated ADSCs. The PD98059 and LY294002 significantly down-regulated the selegiline-induced over-expression of nestin and NF-68; however, PI3K inhibition did not return the genes expression to control level. ADSCs were immunoreactivefor nestin and NF-68 about 98% and 95% respectively. Conclusion: According to the results, selegilinecan induce the gene expression of neural stem cell biomarkers in ADSCs through MAPK pathway activating and so differentiating them into neuron-like cells.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>79</FPAGE>
			<TPAGE>87</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/182020/12/282020/11/14
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/8/24
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/62021/04/102021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Alireza</Name>
				<MidName></MidName>
				<Family>Abdanipour</Family>
				<NameE>Alireza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Abdanipour</FamilyE>
				<Organizations>
				<Organization>Department of Anatomical Sciences, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maedeh</Name>
				<MidName></MidName>
				<Family>Amalavar</Family>
				<NameE>Maedeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Amalavar</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohsen</Name>
				<MidName></MidName>
				<Family>Alipour</Family>
				<NameE>Mohsen</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Alipour</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Hadi</Name>
				<MidName></MidName>
				<Family>Feizi</Family>
				<NameE>Hadi</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Feizi</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>hfeizik@zums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Selegiline</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Adipose-derived stem cells</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Neuron-like cells</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>MAPK.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Abdanipour A, Jafari Anarkooli I, Shokri S, Ghorbanlou M, Bayati V, Nejatbakhsh R. Neuroprotective effects of selegiline on rat neural stem cells treated with hydrogen peroxide. Biomed Rep 2018; 8: 41-6.##Abdanipour A, Tiraihi T, Delshad A. Trans-differentiation of the adipose tissue-derived stem cells into neuron-like cells expressing neurotrophins by selegiline. Iran Biomed J 2011; 15: 113.##Abdanipour A, Tiraihi T. Induction of adipose-derived stem cell into motoneuron-like cells using selegiline as preinducer. Brain Res 2012; 1440: 23-33.##Alhadlaq A, Mao JJ. Mesenchymal stem cells: isolation and therapeutics. Stem Cells Dev 2004; 13: 436-48.##Am OB, Amit T, Youdim M B. Contrasting neuroprotective and neurotoxic actions of respective metabolites of anti-Parkinson drugs rasagiline and selegiline. Neurosci Lett 2004; 355: 169-72.##Amura CR, Marek L, Winn RA, Heasley LE. Inhibited neurogenesis in JNK1-deficient embryonic stem cells. Mol Cell Biol 2005; 25: 10791-802.##Andoh T, Chock PB, Murphy DL, Chiueh C. Role of the redox protein thioredoxin in cytoprotective mechanism evoked by (-)-deprenyl. Mol Pharmacol 2005; 68: 1408-14.##Bai WF, Zhang Y, Xu W, Li W, Li M, Yuan F, et al. Isolation and characterization of neural progenitor cells from bone marrow in cell replacement therapy of brain injury. Front Cell Neurosci 2020; 14: 49.##Boulland JL, Mastrangelopoulou M, Boquest AC, Jakobsen R, Noer A, Glover JC, et al. Epigenetic regulation of nestin expression during neurogenic differentiation of adipose tissue stem cells. Stem Cells Dev 2013; 22: 1042-52.##Cardozo AJ, Gomez DE, Argibay PF. Neurogenic differentiation of human adipose-derived stem cells: relevance of different signaling molecules, transcription factors, and key marker genes. Gene 2012; 511: 427-36.##Creson TK, Yuan P, Manji HK, Chen G. Evidence for involvement of ERK, PI3K, and RSK in induction of Bcl-2 by valproate. J Mol Neurosci 2009; 37: 123-34.##Debnath T, Chelluri LK. Standardization and quality assessment for clinical grade mesenchymal stem cells from human adipose tissue. Hematol Transfus Cell Ther 2019; 41: 7-16.##Dinsmore CJ, Soriano P. MAPK and PI3K signaling: At the crossroads of neural crest development. Dev Biol 2018; 444: S79-97.##Dominici M, Le Blanc K, Mueller I, Slaper-Cortenbach I, Marini F, Krause D, et al. Minimal criteria for defining multipotent mesenchymal stromal cells. The International Society for Cellular Therapy position statement. Cytotherapy 2006; 8: 315-7.##Esmaeili F, Tiraihi T, Movahedin M, Mowla SJ. Selegiline induces neuronal phenotype and neurotrophins expression in embryonic stem cells. Rejuvenation Res 2006; 9: 475-84.##Fan XL, Zhang Y, Li X, Fu QL. Mechanisms underlying the protective effects of mesenchymal stem cell-based therapy. Cell Mol Life Sci 2020; 77: 2771-94.##Fraser JK, Wulur I, Alfonso Z, Hedrick MH. Fat tissue: an underappreciated source of stem cells for biotechnology. Trends Biotechnol 2006; 24: 150-4.##Hong L, Peptan IA, Colpan A, Daw JL. Adipose tissue engineering by human adipose-derived stromal cells. Cells Tissues Organs 2006; 183: 133-40.##Huang T, He D, Kleiner G, Kuluz J. Neuron-like differentiation of adipose-derived stem cells from infant piglets in vitro. J Spinal Cord Med 2007; 30: S35-40.##Huang W, Zhao Y, Zhu X, Cai Z, Wang S, Yao S, et al. Fluoxetine upregulates phosphorylatedAKT and phosphorylated-ERK1/2 proteins in neural stem cells: evidence for a crosstalk between AKT and ERK1/2 pathways. J Mol Neurosci 2013; 49: 244-9.##Isele NB, Lee HS, Landshamer S, Straube A, Padovan CS, Plesnila N, et al. Bone marrow stromal cells mediate protection through stimulation of PI3-K/Akt and MAPK signaling in neurons. Neurochem Int 2007; 50: 243-50.##Kingham PJ, Kalbermatten DF, Mahay D, Armstrong SJ, Wiberg M, Terenghi G. Adiposederived stem cells differentiate into a Schwann cell phenotype and promote neurite outgrowth in vitro. Exp Neurol 2007; 207: 267-74.##Magyar K, Szende B. (-)-Deprenyl, a selective MAO-B inhibitor, with apoptotic and antiapoptotic properties. Neurotoxicology 2004; 25: 233-42.##Mizuno H. Adipose-derived stem cells for tissue repair and regeneration: ten years of research and a literature review. J Nippon Med Sch 2009; 76: 56-66.##Mizuta I, Ohta M, Ohta K, Nishimura M, Mizuta E, Hayashi K, et al. Selegiline and desmethylselegiline stimulate NGF, BDNF, and GDNF synthesis in cultured mouse astrocytes. Biochem Biophys Res Commun 2000; 279: 751-5.##Modrak M, Talukder M A H, Gurgenashvili K, Noble M, Elfar J C. Peripheral nerve injury and myelination: Potential therapeutic strategies. J Neurosci Res 2020; 98: 780-95.##Moelling K, Schad K, Bosse M, Zimmermann S, Schweneker M. Regulation of Raf-Akt Crosstalk. J Biol Chem 2002; 277: 31099-106.##Nakaso K, Nakamura C, Sato H, Imamura K, Takeshima T, Nakashima K. Novel cytoprotective mechanism of anti-parkinsonian drug deprenyl: PI3K and Nrf2-derived induction of antioxidative proteins. Biochem Biophys Res Commun 2006; 339: 915-22.##Naoi M, Maruyama W, Shamoto-Nagai M J J o N T. Rasagiline and selegiline modulate mitochondrial homeostasis, intervene apoptosis system and mitigate α-synuclein cytotoxicity in disease-modifying therapy for Parkinson's disease. J Neural Transm (Vienna). 2020; 127: 131- 47.##Pearson G, Robinson F, Beers Gibson T, Xu B E, Karandikar M, Berman K, et al. Mitogenactivated protein (MAP) kinase pathways: regulation and physiological functions. Endocr Rev 2001; 22: 153-83.##Shan Z Y, Shen J L, Li Q M, Wang Y, Huang X Y, Guo T Y, et al. pCREB is involved in neural induction of mouse embryonic stem cells by RA. Anat Rec (Hoboken) 2008; 291: 519-26.##Sylvester K G, Longaker M T. Stem cells: review and update. Arch Surg 2004; 139: 93-9.##Taheri F, Kashani M, Ghorbanian M, Hosseinpour L. Inductive effect of Deprenyl and Dimethyl sulfoxide on proliferation and survival of the mesenchymal stem cells. J Gorgan Univ Med Sci. 2012; 14: 10-18.##Wang J, Chen Y, Yang Y, Xiao X, Chen S, Zhang C, et al. Endothelial progenitor cells and neural progenitor cells synergistically protect cerebral endothelial cells from Hypoxia/reoxygenation-induced injury via activating the PI3K/Akt pathway. Mol Brain 2016; 9: 12.##Wang X. Stem cells in tissues, organoids, and cancers. Cell Mol Life Sci 2019; 76: 4043-70.##Wei L, Wei Z Z, Jiang M Q, Mohamad O, Yu S P. Stem cell transplantation therapy for multifaceted therapeutic benefits after stroke. Prog Neurobiol 2017; 157: 49-78.##Weinreb O, Amit T, Bar-Am O, Sagi Y, Mandel S, Youdim M. Involvement of multiple survival signal transduction pathways in the neuroprotective, neurorescue and APP processing activity of rasagiline and its propargyl moiety. in, Parkinson's Disease and Related Disorders (Springer). 2006; 70: 457-65##Yuan J, Huang G, Xiao Z, Lin L, Han T J M, biochemistry c. Overexpression of β-NGF promotes differentiation of bone marrow mesenchymal stem cells into neurons through regulation of AKT and MAPK pathway. Mol Cell Biochem 2013; 383: 201-11.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Diethylhexyl phthalate induced oxidative stress and caused metabolic imbalance in bone marrow mesenchymal stem cells</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Diethylhexyl phthalate (DEHP) is leaching form polyvinyl chloride to cause animal toxicity. In our previous study, DEHP caused osteoblasts mortality in vitro, since rat bone marrow mesenchymal stem cells (MSCs) is the cellular back up for osteoblasts; therefore its effect on MSCs was investigated. Methods: MSCs were extracted from Westar rats and treated with 0.5 to 2500&#956;M of DEHP for 12, 24 and 48h to study the viability. Then further investigations, including proliferation, cell morphology, sodium and potassium level, concentration of calcium, total protein, activity of metabolic enzymes (ALT, AST, ALP, LDH), malondialdehyde (MDA) level, total antioxidant capacity, activity of superoxide dismutase (SOD) and catalase (CAT) were measured using selected concentration (100, 500 and 1500&#956;M). Results: The 100&#956;M of DEHP did not change the viability and biochemical factor after 48h but colony forming assay and population doubling number was significantly affected. Th 500&#956;M only reduced the viability at 24 and 48h, while 1500&#956;M caused the significant reduction at all the periods. These two concentrations, caused significant proliferation reduction as well as significant increase in calcium and sodium level, LDH activity and MDA level. In addition, we observed decrease in potassium, total protein, activity of metabolic enzymes and activity of CAT and SOD significantly. Conclusion: DEHP has reduced viability and proliferation of MSCs through metabolic change, alteration in cellular ultrastructure, ionic imbalance and induction of oxidative stress.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>88</FPAGE>
			<TPAGE>100</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/182020/12/282020/11/142020/11/27
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/9/7
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/62021/04/102021/04/62021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mohammad Hussein</Name>
				<MidName></MidName>
				<Family>Abnosi</Family>
				<NameE>Mohammad Hussein</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Abnosi</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Faculty of Sciences, Arak University, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>m-abnosi@araku.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Zahra</Name>
				<MidName></MidName>
				<Family>Aliyari Babolghani</Family>
				<NameE>Zahra</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Aliyari Babolghani</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Faculty of Sciences, Arak University, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Mesenchymal Stem Cell</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Diethylhexyl phthalate</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Oxidative stress</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Cell survival</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Enzymes assay.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Abnosi MH, Aliyari Babolghani Z. The Inhibitory Role of Di-2-ethylhexyl phthalate on osteogenic differentiation of mesenchymal stem cells via down-regulation of runx2 and membrane function impairment. Int J Med Toxicol Forensic Med 2020; 10: 26673.##Abnosi MH, Yari S. The toxic effect of gallic acid on biochemical factors, viability and proliferation of rat bone marrow mesenchymal stem cells was compensated by boric acid. J Trace Elem Med Biol 2018; 48: 246-53.##Alto P. Plasticizers. Chemical Economics Handbook. Stanford Research Associates (SRI) International, CA. USA. 1996.##Ambruosi B, Uranio MF, Sardanelli AM, Pocar P, Martino NA, Paternoster MS, et al. In vitro acute exposure to DEHP affects oocyte meiotic maturation, energy and oxidative stress parameters in a large animal model. PLoS One 2011; 6: e27452.##Ashari S, Karami M, Shokrzadeh M, Ghandadi M, Ghassemi-Barghi N, Dashti A, et al. The implication of mitochondrial dysfunction and mitochondrial oxidative damage in di (2- ethylhexyl) phthalate induced nephrotoxicity in both in vivo and in vitro models. Toxicol Mech Methods 2020; 30: 427-37.##Autian J. Toxicity and health threats of phthalate esters: review of the literature. Environ health perspect 1973; 4: 3-26.##AuBuchon JP, Estep TN, Davey RJ. The effect of the plasticizer Diethylhexyl phthalate on the survival of stored RBCs. Blood 1988; 71: 448-52.##Berridge MJ, Bootman MD, Roderick HL. Calcium signalling: dynamics, homeostasis and remodelling. Nat Rev Mol Cell Biol 2003; 4: 517-29.##Bhat FA, Ramajayam G, Parameswari S, Vignesh RC, Karthikeyan S, Senthilkumar K, et al. Di 2-ethyl hexyl phthalate affects differentiation and matrix mineralization of rat calvarial osteoblasts-in vitro. Toxicol in Vitro 2013; 27: 250-56.##Chiu CY, Sun SC, Chiang CK, Wang CC, Chan DC, Chen HJ, et al. Plasticizer di (2-ethylhexyl) phthalate interferes with osteoblastogenesis and adipogenesis in a mouse. Model J Orthop Res 2018; 26: 1124-34.##De Sousa EB, Casado PL, Neto VM, Leite Duarte ME, Aguiar DP. Synovial fluid and synovial membrane mesenchymal stem cells: latest discoveries and herapeutic perspectives. Stem Cell Res Ther 2014; 5: 112.##Dhanya CR, Indu AR, Deepadevi KV, Kurup PA. Inhibition of membrane Na+-K+ ATPase of the brain, liver and RBC in rats administered di (2-ethyl hexyl) phthalate (DEHP) a plasticizer used in polyvinyl chloride (PVC) blood storage bags. Indian J Exp Biol 2003; 41: 814-20.##Eslaminejad MB. Mesenchymal stem cell: isolation and biology. J Iranian Anatom Sci 2007; 5: 61-73.##Gross SR, Kinzy TG. Improper organization of the actin cytoskeleton affects protein synthesis at initiation. Mol Cell Biol 2007; 27: 1974-89.##Gu Y, Gao M, Zhang W, Yan L, Shao F, Zhou J. Exposure to phthalates DEHP and DINP May lead to oxidative damage and lipidomic disruptions in mouse kidney. Chemosphere 2021; 271: 129740.##Hajnóczky G, Csordás G, Das S, Garcia-Perez C, Saotome M, Roy SS, et al. Mitochondrial calcium signalling and cell death: approaches for assessing the role of mitochondrial Ca 2+ uptake in apoptosis. Cell Calcium 2006; 40: 553-60.##Hillman LS, Goodwin SL, Sherman WR. Identification and measurement of plasticizer in neonatal tissues after umbilical catheters and blood products. N Engl J Med 1975; 292: 381-6.##Huber WW, Grasl-Kraupp, B, Schulte-Hermann R. Hepatocarcinogenic potential of di (2- ethylhexyl) phthalate in rodents and its implications on human risk. Crit Rev Toxicol 1996; 26: 365-81.##Hucho T, Levine JD. Signaling pathways in sensitization: toward a nociceptor cell biology. Neuron 2007; 55: 365-76.##International Programme on Chemical Safety (IPCS). 1992. Environmental health criteria 131: diethylhexyl phthalate. 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Distribution of di (2-ethylhexyl) phthalate and products in blood and blood components. Environ Health Perspect 1986; 65: 309-16.##Sabbieti MG, Agas D, Santoni G, Materazzi S, Menghi G, Marchetti L. Involvement of p53 in phthalate effects on mouse and rat osteoblasts. J Cell Biochem 2009; 107: 316-27.##Siddiqui A, Srivastava SP. Effect of di (2-ethylhexyl) phthalate administration on rat sperm count and on sperm metabolic enzymes. Bull Environ Contam Toxicol 1992; 48: 115-19.##Singh Rowdhwal SS, Chen J. Toxic effects of Di-2-ethylhexyl Phthalate: an overview. Biomed Res Int 2018.##European :union: risk assessment report bis-(2-ethylhexyl) phthalate (DEHP). 2008; VOL 80, 2nd priority list. Sweden.##Tripathi A, Pandey V, Sahu AN, Singh A, Dubey PK. Di-(2-ethylhexyl) phthalate (DEHP) inhibits steroidogenesis and induces mitochondria-ROS mediated apoptosis in rat ovarian granulosa cells. Toxicol Res 2019; 8: 381-94.##Wang Y, Wang T, Ban Y, Shen C, Shen Q, Chai X, et al. Di-(2-ethylhexyl) Phthalate exposure modulates antioxidant enzyme activity and gene expression in juvenile and adult daphnia magna. Arch Environ Contam Toxicol 2018; 75: 145-56.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Corrigendum to “Antioxidant activity, phenolic and flavonoid content of Lawsonia inermis and Haplophyllum vermiculare” [Physiol Pharmacol 25 (2021) 261-269]</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Continuous exposure of oxidants to the skin may disrupt the antioxidant balance and leads to inflammatory skin diseases (ISD). The aim of the present study was to compare the antioxidant activity, phenolic and flavonoid content of two traditionally used plants in ISD, Lawsonia inermis and Haplophyllum vermiculare.
Methods: The hydroethanolic extract of the plants was prepared by maceration. Phenolic and flavonoid content of the extracts was measured respectively with Folin-Ciocateu and aluminum chloride methods. The monovalent reducing power and radical scavenging activity were also evaluated respectively by ferric reducing antioxidant power and 2,2-diphenyl-1-picryl-hydrazyl methods.
Results: The reducing power of Lawsonia inermis (862.89&#177;32.23 &#956;molFe2+/g) was significantly higher than Haplophyllum vermiculare extract (765.52&#177;29.39 &#956;molFe2+/g). The radical scavenging activity of Lawsonia inermis extract at a concentration of 1000&#956;g/ml (%65.72&#177;0.77) was also significantly higher than Haplophyllum vermiculare (%36.34&#177;2.52). The higher antioxidant activity of Lawsonia inermis is probably due to its higher phenolic (96.76&#177;3.34&#956;g GAE/mg) and flavonoid content (197.69&#177;5.76&#956;g QE/mg).
Conclusion: Henna leaves had higher antioxidant activity, phenolic and flavonoid content compared to aerial parts of Haplophyllum vermiculare, and may be more effective in improving oxidative stress, prevention and treatment of ISD.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>101</FPAGE>
			<TPAGE>101</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/182020/12/282020/11/142020/11/272022/03/16
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1400/12/25
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/62021/04/102021/04/62021/04/62022/03/16
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/12/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Alireza</Name>
				<MidName></MidName>
				<Family>Moulazadeh</Family>
				<NameE>Alireza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Moulazadeh</FamilyE>
				<Organizations>
				<Organization>Noncommunicable Disease Research Center, Fasa University of Medical Sciences, Fasa, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Seyyed Amin</Name>
				<MidName></MidName>
				<Family>kouhpayeh</Family>
				<NameE>Seyyed Amin</NameE>
				<MidNameE></MidNameE>
				<FamilyE>kouhpayeh</FamilyE>
				<Organizations>
				<Organization>Noncommunicable Disease Research Center, Fasa University of Medical Sciences, Fasa, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Razieh</Name>
				<MidName></MidName>
				<Family>Ranjbar</Family>
				<NameE>Razieh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ranjbar</FamilyE>
				<Organizations>
				<Organization>Noncommunicable Disease Research Center, Fasa University of Medical Sciences, Fasa, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Amin</Name>
				<MidName></MidName>
				<Family>Dakhili Ardestani</Family>
				<NameE>Amin</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Dakhili Ardestani</FamilyE>
				<Organizations>
				<Organization>Student Research Committee, Fasa University of Medical Sciences, Fasa, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maryam</Name>
				<MidName></MidName>
				<Family>Hekmat</Family>
				<NameE>Maryam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Hekmat</FamilyE>
				<Organizations>
				<Organization>Student Research Committee, Fasa University of Medical Sciences, Fasa, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Sara</Name>
				<MidName></MidName>
				<Family>Azarnia</Family>
				<NameE>Sara</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Azarnia</FamilyE>
				<Organizations>
				<Organization>Noncommunicable Disease Research Center, Fasa University of Medical Sciences, Fasa, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Sohrab</Name>
				<MidName></MidName>
				<Family>Najafipour</Family>
				<NameE>Sohrab</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Najafipour</FamilyE>
				<Organizations>
				<Organization>Medicinal Plant Research Center, Fasa University of Medical Sciences, Fasa, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>Najafipour.s@fums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Lawsonia inermis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Haplophyllum vermiculare</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Antioxidative activity</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Skin disease</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Inflammation</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>

</ARTICLES>

</JOURNAL>
</XML>
