<?xml version="1.0" encoding="utf-8"?>
<XML>
<JOURNAL>
<YEAR>2020</YEAR>
<VOL>24</VOL>
<NO>1</NO>
<MOSALSAL>76</MOSALSAL>
<PAGE_NO>81</PAGE_NO>


<ARTICLES>

	<ARTICLE> 
		<TitleF>Long non‐coding RNA Miat mediates cross-talk between the kidneys and hippocampus in the rat model of acute kidney injury</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The role of long noncoding RNAs (lncRNAs) has been intensively studied in the development of several human diseases. Myocardial infarction-associated transcript (Miat) is among the most abundant and highly conserved lncRNAs that exhibits deregulation in some critical diseases. However, it remains unclear whether Miat may also play a role in the pathogenesis of acute kidney injury (AKI) and neurological consequences. Methods: In the present study, the expression of lncRNA Miat was measured in the rat kidney and hippocampus tissues to assess if there is an association between the expression of it and AKI. AKI was induced by clamping the bilateral renal artery for 45min and was confirmed 24 hours after reperfusion by biochemical markers and histopathological assessments in rat kidneys. Results: We observed an increasing trend of Miat expression (256-fold) in the kidney as well as the hippocampus (2-fold) following AKI. Conclusion: It appears that there is a relationship between the deregulation of the Miat expression and AKI and the hippocampal involvement, although more studies are needed to confirm the functional effect of this lncRNA in AKI.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>1</FPAGE>
			<TPAGE>9</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/27
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1398/1/7
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/24
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/6/2
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Maryam</Name>
				<MidName></MidName>
				<Family>Malek</Family>
				<NameE>Maryam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Malek</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>malek.maryam@med.mui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Farnaz</Name>
				<MidName></MidName>
				<Family>Mohammadtaheri</Family>
				<NameE>Farnaz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mohammadtaheri</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Faculty of Basic Sciences, Shahrekord University, Shahrekord, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Parvaneh</Name>
				<MidName></MidName>
				<Family>Nikpour</Family>
				<NameE>Parvaneh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Nikpour</FamilyE>
				<Organizations>
				<Organization>Department of Genetics and Molecular Biology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Azar</Name>
				<MidName></MidName>
				<Family>Baradaran</Family>
				<NameE>Azar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Baradaran</FamilyE>
				<Organizations>
				<Organization>Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Long non‐coding RNA</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Miat</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Acute kidney injury</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Hippocampus.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Albertson DN, Schmidt CJ, Kapatos G, Bannon MJ. Distinctive profiles of gene expression in the human nucleus accumbens associated with cocaine and heroin abuse. Neuropsychopharmacology 2006; 31: 2304-12. DOI: 10.1038/sj.npp.1301089. ##Barry G, Briggs JA, Vanichkina DP, Poth EM, Beveridge NJ, Ratnu VS, et al. The long non-coding RNA Gomafu is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing. Mol Psychiatry 2014; 19: 486-94. DOI: 10.1038/mp.2013.45 ##Blackshaw S, Harpavat S, Trimarchi J, Cai L, Huang H, Kuo WP, et al. Genomic analysis of mouse retinal development. PLoS Biol 2004; 2: E247. DOI: 10.1371/journal.pbio.0020247 ##Bugnicourt JM, Godefroy O, Chillon JM, Choukroun G, Massy ZA. Cognitive disorders and dementia in CKD: the neglected kidney-brain axis. J Am Soc Nephrol 2013; 24: 353-63. DOI: 10.1681/ASN.2012050536 ##Burn DJ, Bates D. Neurology and the kidney. J Neurol Neurosurg Psychiatry 1998; 65: 810-21. DOI: 10.1136/ jnnp.65.6.810 ##Carpenter S, Aiello D, Atianand MK, Ricci EP, Gandhi P, Hall LL, et al. A long noncoding RNA mediates both activation and repression of immune response genes. Science 2013; 341: 789-92. DOI: 10.1126/ science.1240925 ##Chen YG, Satpathy AT, Chang HY. Gene regulation in the immune system by long noncoding RNAs. Nat Immunol 2017; 18: 962-972. DOI: 10.1038/ni.3771 ##Chou AH, Lee CM, Chen CY, Liou JT, Liu FC, Chen YL, et al. Hippocampal transcriptional dysregulation after renal ischemia and reperfusion. Brain Res 2014; 1582: 197-210. DOI: 0.1016/j.brainres.2014.07.030 ##De Deyn PP, Saxena VK, Abts H, Borggreve F, D'Hooge R, Marescau B, et al. Clinical and pathophysiological aspects of neurological complications in renal failure. Acta Neurol Belg 1992; 92: 191-206. ##Doi K, Rabb H. Impact of acute kidney injury on distant organ function: recent findings and potential therapeutic targets. Kidney Int 2016; 89: 555-64. DOI: 10.1016/ j.kint.2015.11.019 ##Fenoglio C, Ridolfi E, Galimberti D, Scarpini E. An emerging role for long non-coding RNA dysregulation in neurological disorders. Int J Mol Sci 2013; 14: 20427-42. DOI: 10.3390/ijms141020427 ##Heward JA, Lindsay MA. Long non-coding RNAs in the regulation of the immune response. Trends Immunol 2014; 35: 408-19. DOI: 10.1016/j.it.2014.07.005 ##Ilott NE, Heward JA, Roux B, Tsitsiou E, Fenwick PS, Lenzi L, et al. Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes. Nat commun 2014; 5: 3979. DOI: 10.1038/ncomms7814 ##Ishii N, Ozaki K, Sato H, Mizuno H, Saito S, Takahashi A, et al. Identification of a novel non-coding RNA, MIAT, that confers risk of myocardial infarction. J Hum Genet 2006; 51: 1087-99. DOI: 10.1007/s10038-006-0070-9 ##Kao CC, Wu CH, Lai CF, Huang TM, Chen HH, Wu VC, et al. Long-term risk of dementia following acute kidney injury: a population-based study. Ci Ji Yi Xue Za Zhi 2017; 29: 201-207. DOI: 10.4103/tcmj.tcmj_40_17 ##Kovalčíková A, Gyurászová M, Vavrincová-Yaghi D, Vavrinec P, Tóthová Ľ, Boor P, et al. Oxidative stress in the brain caused by acute kidney injury. Metab Brain Dis 2018; 33: 961-967. DOI: 10.1007/s11011-018-0204-8 ##Liao J, He Q, Li M, Chen Y, Liu Y, Wang J. LncRNA MIAT: myocardial infarction associated and more. Gene 2016; 578: 158-61. DOI: 10.1016/j.gene.2015.12.032 ##Lin J, Zhang X, Xue C, Zhang H, Shashaty MG, Gosai SJ, et al. The long noncoding RNA landscape in hypoxic and inflammatory renal epithelial injury. Am J of Physiol Renal Physiol 2015; 309: F901-F13. DOI: 10.1152/ajprenal.00290.2015 ##Liu M, Liang Y, Chigurupati S, Lathia JD, Pletnikov M, Sun Z, et al. Acute kidney injury leads to inflammation and functional changes in the brain. J Am Soc Nephrol 2008; 19: 1360-70. DOI: 10.1681/ASN.2007080901 ##Liu T, Zhang L, Joo D, Sun SC. NF-κB signaling in inflammation. Signal Transduct Target Ther 2017; 2: 17023. DOI: 10.1038/sigtrans.2017.23 ##Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods 2001; 25: 402-8. DOI: 10.1006/meth.2001.1262 ##Logsdon AF, Lucke-Wold BP, Turner RC, Huber JD, Rosen CL, Simpkins JW. Role of microvascular disruption in brain damage from traumatic brain injury. Compr Physiol 2015; 5: 1147-60. DOI: 10.1002/cphy.c140057 ##Lorenzen JM, Thum T. Long noncoding RNAs in kidney and cardiovascular diseases. Nat Rev Nephrol 2016; 12: 360-73. DOI: 10.1038/nrneph.2016.51 ##Lu R, Kiernan MC, Murray A, Rosner MH, Ronco C. Kidney-brain crosstalk in the acute and chronic setting. Nat Rev Nephrol 2015; 11: 707-19. DOI: 10.1038/nrneph.2015.131 ##Malek M, Nematbakhsh M. The preventive effects of diminazene aceturate in renal ischemia/reperfusion injury in male and female rats. Adv Prev Med 2014; 2014: 740647. DOI: 10.1155/2014/740647 ##Mathy NW, Chen X-M. Long non-coding RNAs (lncRNAs) and their transcriptional control of inflammatory responses. J Biol Chem 2017; 292: 12375-12382. DOI: 10.1074/jbc.R116.760884 ##Mirza AH, Berthelsen CH, Seemann SE, Pan X, Frederiksen KS, Vilien M, et al. Transcriptomic landscape of lncRNAs in inflammatory bowel disease. Genome med 2015; 7: 39. DOI: 10.1186/s13073-015-0162-2 ##Nasrollahzadeh-Khakiani M, Emadi-Baygi M, Nikpour P. Augmented expression levels of lncRNAs ecCEBPA and UCA1 in gastric cancer tissues and their clinical significance. Iran J Basic Med Sci 2017a; 20: 1149-58. DOI: 10.22038/IJBMS.2017.9448 ##Nasrollahzadeh-Khakiani M, Emadi-Baygi M, Schulz WA, Nikpour P. Long noncoding RNAs in gastric cancer carcinogenesis and metastasis. Brief Funct Genomics 2017b; 16: 129-45. doi: 10.1093/bfgp/elw011 ##Niland CN, Merry CR, Khalil AM. Emerging roles for long non-coding RNAs in cancer and neurological disorders. Front Genet 2012; 3: 25. DOI: 10.3389/ fgene.2012.00025 ##Nongnuch A, Panorchan K, Davenport A. Brain-kidney crosstalk. Critical care 2014; 18: 225. DOI: 10.1186/cc13907 ##Ohnishi Y, Tanaka T, Yamada R, Suematsu K, Minami M, Fujii K, et al. Identification of 187 single nucleotide polymorphisms (SNPs) among 41 candidate genes for ischemic heart disease in the Japanese population. Hum Genet 2000; 106: 288-92. DOI: 10.1007/ s004390051039 ##Puthanveetil P, Chen S, Feng B, Gautam A, Chakrabarti S. Long non-coding RNA MALAT1 regulates hyperglycaemia induced inflammatory process in the endothelial cells. J Cell Mol Med 2015; 19: 1418-25. DOI: 10.1111/jcmm.12576 ##Rabb H, Griffin MD, McKay DB, Swaminathan S, Pickkers P, Rosner MH, et al. Inflammation in AKI: current understanding, key questions, and knowledge gaps. J Am Soc Nephrol 2016; 27: 371-9. DOI: 10.1681/ASN.2015030261 ##Reddy MA, Chen Z, Park JT, Wang M, Lanting L, Zhang Q, et al. Regulation of inflammatory phenotype in macrophages by a diabetes-induced long noncoding RNA. Diabetes 2014; 63: 4249-61. DOI: 10.2337/db14-0298 ##Salvadori M, Rosso G, Bertoni E. Update on ischemia-reperfusion injury in kidney transplantation: pathogenesis and treatment. World J Transplant 2015; 5: 52-67. DOI: 10.5500/wjt.v5.i2.52 ##Shiao CC, Wu PC, Huang TM, Lai TS, Yang WS, Wu CH, et al. Long-term remote organ consequences following acute kidney injury. Crit Care 2015; 19: 438. DOI: 10.1186/s13054-015-1149-5 ##Sone M, Hayashi T, Tarui H, Agata K, Takeichi M, Nakagawa S. The mRNA-like noncoding RNA Gomafu constitutes a novel nuclear domain in a subset of neurons. J Cell Sci 2007; 120: 2498-506. DOI: 10.1242/jcs.009357 ##Sun C, Huang L, Li Z, Leng K, Xu Y, Jiang X, et al. Long non-coding RNA MIAT in development and disease: a new player in an old game. J Biomed Sci 2018; 25: 23. DOI: 10.1186/s12929-018-0427-3 ##Sutton TA. Alteration of microvascular permeability in acute kidney injury. Microvasc Res 2009; 77: 4-7. DOI: 10.1016/j.mvr.2008.09.004 ##Sutton TA, Fisher CJ, Molitoris BA. Microvascular endothelial injury and dysfunction during ischemic acute renal failure. Kidney Int 2002; 62: 1539-49. DOI: 10.1046/j.1523-1755.2002.00631.x ##Tsai HH, Yen RF, Lin CL, Kao CH. Increased risk of dementia in patients hospitalized with acute kidney injury: A nationwide population-based cohort study. PloS one 2017; 12: e0171671. DOI: 10.1371/ journal.pone.0171671 ##Yan B, Yao J, Liu JY, Li XM, Wang XQ, Li YJ, et al. lncRNA-MIAT regulates microvascular dysfunction by functioning as a competing endogenous RNA. Circ Res 2015; 116: 1143-56. DOI: 10.1161/CIRCRESAHA. 116.305510 ##Yang H, Liang N, Wang M, Fei Y, Sun J, Li Z, et al. Long noncoding RNA MALAT-1 is a novel inflammatory regulator in human systemic lupus erythematosus. Oncotarget 2017; 8: 77400. DOI: 10.18632/ oncotarget.20490 ##Yap SC, Lee HT. Acute kidney injury and extrarenal organ dysfunction: new concepts and experimental evidence. Anesthesiology 2012; 116: 1139-48. DOI: 10.1097/ALN.0b013e31824f951b ##Zhang J, Chen M, Chen J, Lin S, Cai D, Chen C, et al. Long non-coding RNA MIAT acts as a biomarker in diabetic retinopathy by absorbing miR-29b and regulating cell apoptosis. Biosci Rep 2017; 37: BSR20170036. DOI: 10.1042/BSR20170036 ##Zhou L, Xu DY, Sha WG, Shen L, Lu GY, Yin X. Long non-coding MIAT mediates high glucose-induced renal tubular epithelial injury. Biochem Biophys Res Commun 2015; 468: 726-32. DOI: 10.1016/j.bbrc.2015.11.023 ##Zhou X, Han X, Wittfeldt A, Sun J, Liu C, Wang X, et al. Long non-coding RNA ANRIL regulates inflammatory responses as a novel component of NF-κB pathway. RNA Biol 2016; 13: 98-108. DOI: 10.1080/15476286. 2015.1122164 ##Zhu M, Li N, Luo P, Jing W, Wen X, Liang C, et al. Peripheral blood leukocyte expression of lncRNA MIAT and its diagnostic and prognostic value in ischemic stroke. J Stroke Cerebrovasc Dis 2018; 27: 326-337. DOI: 10.1016/j.jstrokecerebrovasdis.2017.09.009## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Protective effect of nobiletin against apoptosis induced by 6-hydroxydoamine in human neuroblastoma cells</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Parkinson&#39;s disease (PD) is the second most common neurodegenerative disorder characterized by the damage of dopaminergic neurons of substantia nigra. Despite considerable research, therapeutic approaches aimed at the prevention and long-term treatment of PD have not been quite successful. Therefore, there is a tendency for the identification of novel medical intervention derived from natural substances. Nobiletin, an important citrus flavonoid commonly present in sweet and bitter orange peel, has been suggested to act as a neuroprotective agent in animal models of PD. This study was aimed to assess the potentials of nobiletin in preventing neuronal death and caspase-3 in SH-SY5Y cells. Methods: SH-SY5Y cells were grown in DMEM/F12 media supplemented with 10% fetal bovine serum. The 6-hydroxydopamine (6-OHDA) with or without nobiletin was added to cells. After 24h, the cells were examined for morphological changes under a light microscope and viability by MTT assay. The protective doses of nobiletin was chosen through a pilot study and accordingly the doses 50 and 250&#956;M were selected for further assessments. Western blot assays were done to examine the effect of 6-OHDA with/without nobiletin on cleaved (active) caspase-3. Results: Our results showed that nobiletin is effective in attenuating the effect of 6-OHDA on cell viability by the MTT assay. Nobiletin also reduced the cleavage of caspase-3 induced by 6-OHDA. Conclusion: These results suggest that nobiletin has protective effects against dopaminergic neural toxicity and its anti-apoptotic effect is involved, at least in part, in such protection.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>10</FPAGE>
			<TPAGE>18</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/272019/06/10
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1398/3/20
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/242019/10/5
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/7/13
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Roksana</Name>
				<MidName></MidName>
				<Family>SoukhakLari</Family>
				<NameE>Roksana</NameE>
				<MidNameE></MidNameE>
				<FamilyE>SoukhakLari</FamilyE>
				<Organizations>
				<Organization>Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Majid Reza</Name>
				<MidName></MidName>
				<Family>Farokhi</Family>
				<NameE>Majid Reza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Farokhi</FamilyE>
				<Organizations>
				<Organization>Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maryam</Name>
				<MidName></MidName>
				<Family>Moosavi</Family>
				<NameE>Maryam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Moosavi</FamilyE>
				<Organizations>
				<Organization>Nanobiology and Nanomedicine Research Centre, Shiraz University of Medical sciences, Shiraz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>marmoosavi@sums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Nobiletin</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>SH-SY5Y</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Caspase-3</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Cell viability</KeyText>
			</KEYWORD>

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

		<REFRENCES>
			<REFRENCE>
				<REF>Amiri E, Ghasemi R, Moosavi M. Agmatine protects against 6-ohda-induced apoptosis, and erk and akt/gsk disruption in sh-sy5y cells. Cell Mol Neurobiol 2016; 36: 829-838. DOI: 10.1007/s10571-015-0266-7. ##Blum D, Torch S, Lambeng N, Nissou M, Benabid AL, Sadoul R, et al. Molecular pathways involved in the neurotoxicity of 6-ohda, dopamine and mptp: Contribution to the apoptotic theory in parkinson's disease. Prog Neurobiol 2001; 65: 135-72. DOI: 10.1016/s0301-0082(01)00003-x. ##Braidy N, Behzad S, Habtemariam S, Ahmed T, Daglia M, Nabavi SM, et al. Neuroprotective effects of citrus fruit-derived flavonoids, nobiletin and tangeretin in alzheimer's and parkinson's disease. CNS Neurol Disord Drug Targets 2017; 16: 387-397. DOI: 10.2174/1871527316666170328113309. ##Chaudhry ZL, Ahmed BY. Caspase-2 and caspase-8 trigger caspase-3 activation following 6-ohda-induced stress in human dopaminergic neurons differentiated from renvm stem cells. Neurol Res 2013; 35: 435-40. DOI: 10.1179/1743132812y.0000000135. ##Cohen GM. Caspases: The executioners of apoptosis. Biochem J 1997; 326 ( Pt 1): 1-16. DOI: 10.1042/ bj3260001. ##Cui Y, Wu J, Jung SC, Park DB, Maeng YH, Hong JY, et al. Anti-neuroinflammatory activity of nobiletin on suppression of microglial activation. Biol Pharm Bull 2010; 33: 1814-21. DOI: 10.1248/bpb.33.1814. ##Datta SR, Dudek H, Tao X, Masters S, Fu H, Gotoh Y, et al. Akt phosphorylation of bad couples survival signals to the cell-intrinsic death machinery. Cell 1997; 91: 231-241. DOI: 10.1016/s0092-8674(00)80405-5. ##Dodel RC, Du Y, Bales KR, Ling Z, Carvey PM, Paul SM. Caspase-3-like proteases and 6-hydroxydopamine induced neuronal cell death. Brain Res Mol Brain Res 1999; 64: 141-8. DOI: 10.1016/s0169-328x(98)00318-0 ##Dorszewska J, Prendecki M, Lianeri M, Kozubski W. Molecular effects of l-dopa therapy in parkinson's disease. Curr Genomics 2014; 15: 11-7. DOI: 10.2174/1389202914666131210213042. ##Ferger B, Rose S, Jenner A, Halliwell B, Jenner P. 6-hydroxydopamine increases hydroxyl free radical production and DNA damage in rat striatum. NeuroReport 2001; 12: 1155-1159. ##Forno LS. Neuropathology of parkinson's disease. J Neuropathol Exp Neurol 1996; 55: 259-72. ##Gu M, Cooper JM, Taanman JW, Schapira AH. Mitochondrial DNA transmission of the mitochondrial defect in parkinson's disease. Ann Neurol 1998; 44: 177-86. DOI: 10.1002/ana.410440207. ##Hartmann A, Hunot S, Michel PP, Muriel MP, Vyas S, Faucheux BA, et al. Caspase-3: a vulnerability factor and final effector in apoptotic death of dopaminergic neurons in parkinson's disease. Proc Natl Acad Sci U S A 2000; 97: 2875-80. DOI: 10.1073/pnas.040556597. ##He Y, Lee T, Leong SK. 6-hydroxydopamine induced apoptosis of dopaminergic cells in the rat substantia nigra. Brain Res 2000; 858: 163-166. DOI: 10.1016/s0006-8993(99)02459-2. ##Howard S, Bottino C, Brooke S, Cheng E, Giffard RG, Sapolsky R. Neuroprotective effects of bcl-2 overexpression in hippocampal cultures: interactions with pathways of oxidative damage. J Neurochem 2002; 83: 914-23. DOI: 10.1046/j.1471-4159.2002.01198.x. ##Huang H, Li L, Shi W, Liu H, Yang J, Yuan X, et al. The multifunctional effects of nobiletin and its metabolites in vivo and in vitro. Evid-Based Complementary Altern Med 2016; 2016: 2918796-2918796. DOI: 10.1155/ 2016/2918796. ##Hwang O. Role of oxidative stress in parkinson's disease. Exp Neurobiol 2013; 22: 11-7. DOI: 10.5607/en. 2013.22.1.11. ##Ikeda Y, Tsuji S, Satoh A, Ishikura M, Shirasawa T, Shimizu T. Protective effects of astaxanthin on 6-hydroxydopamine-induced apoptosis in human neuroblastoma sh-sy5y cells. J Neurochem 2008; 107: 1730-1740. DOI: 10.1111/j.1471-4159.2008.05743.x. ##Jeong KH, Jeon MT, Kim HD, Jung UJ, Jang MC, Chu JW, et al. Nobiletin protects dopaminergic neurons in the 1-methyl-4-phenylpyridinium-treated rat model of parkinson's disease. J Med Food 2015; 18: 409-14. DOI: 10.1089/jmf.2014.3241. ##Khan S, Ahmad K, Alshammari EM, Adnan M, Baig MH, Lohani M, et al. Implication of caspase-3 as a common therapeutic target for multineurodegenerative disorders and its inhibition using nonpeptidyl natural compounds. BioMed Res Int 2015; 2015: 379817. DOI: 10.1155/2015/379817. ##Kingsbury AE, Mardsen CD, Foster OJ. DNA fragmentation in human substantia nigra: apoptosis or perimortem effect? Mov Disord 1998; 13: 877-84. DOI: 10.1002/ mds.870130604. ##Lees AJ, Hardy J, Revesz T. Parkinson's disease. Lancet 2009; 373: 2055-66. DOI: 10.1016/S0140-6736(09) 60492-X. ##Li ZR, Yang L, Zhen J, Zhao Y, Lu ZN. Nobiletin protects pc12 cells from ers-induced apoptosis in ogd/r injury via activation of the pi3k/akt pathway. Exp Ther Med 2018; 16: 1470-1476. DOI: 10.3892/etm.2018.6330. ##Liu L, Wu XW. Nobiletin protects human retinal pigment epithelial cells from hydrogen peroxide-induced oxidative damage. J Biochem Mol Toxicol 2018; 32: e22052. DOI: 10.1002/jbt.22052. ##Ljungdahl A, Hokfelt T, Jonsson G, Sachs C. Autoradiographic demonstration of uptake and accumulation of 3h-6-hydroxydopamine in adrenergic nerves. Experientia 1971; 27: 297-9. DOI: 10.1007/ bf02138157. ##Lotharius J, Dugan LL, O'Malley KL. Distinct mechanisms underlie neurotoxin-mediated cell death in cultured dopaminergic neurons. J Neurosci 1999; 19: 1284-93. doi: 10.1523/JNEUROSCI.19-04-01284.1999. ##Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the folin phenol reagent. J Biol Chem 1951; 193: 265-75. ##Mao Q, Liang X, Wu Y, Lu Y. Nobiletin protects against myocardial injury and myocardial apoptosis following coronary microembolization via activating pi3k/akt pathway in rats. Naunyn-Schmiedeberg Arch of Pharmacol 2019. DOI: 10.1007/s00210-019-01661-y. ##Moosavi M, Farrokhi MR, Tafreshi N. The effect of curcumin against 6-hydroxydopamine induced cell death and akt/gsk disruption in human neuroblastoma cells. Physiol Pharmacol 2018; 22: 163-171. ##Nemoto K, Ikeda A, Yoshida C, Kimura J, Mori J, Fujiwara H, et al. Characteristics of nobiletin-mediated alteration of gene expression in cultured cell lines. Biochem Biophys Res Commun 2013; 431: 530-4. DOI: 10.1016/j.bbrc.2013.01.024. ##Onozuka H, Nakajima A, Matsuzaki K, Shin RW, Ogino K, Saigusa D, et al. Nobiletin, a citrus flavonoid, improves memory impairment and abeta pathology in a transgenic mouse model of alzheimer's disease. J Pharmacol Exp Ther 2008; 326: 739-44. DOI: 10.1124/jpet.108.140293. ##Perier C, Bove J, Vila M. Mitochondria and programmed cell death in parkinson's disease: apoptosis and beyond. Antioxid Redox Signal 2012; 16: 883-95. DOI: 10.1089/ars.2011.4074. ##Salakou S, Kardamakis D, Tsamandas AC, Zolota V, Apostolakis E, Tzelepi V, et al. Increased bax/bcl-2 ratio up-regulates caspase-3 and increases apoptosis in the thymus of patients with myasthenia gravis. In Vivo 2007; 21: 123-32. no DOI. ##Sasaki K, Yoshizaki F. Nobiletin as a tyrosinase inhibitor from the peel of citrus fruit. Biol Pharm Bull 2002; 25: 806-8. DOI: 10.1248/bpb.25.806. ##Song JX, Shaw PC, Wong NS, Sze CW, Yao XS, Tang CW, et al. Chrysotoxine, a novel bibenzyl compound selectively antagonizes mpp(+), but not rotenone, neurotoxicity in dopaminergic sh-sy5y cells. Neurosci Lett 2012; 521: 76-81. DOI: 10.1016/j.neulet. 2012.05.063. ##Sookhaklari R, Geramizadeh B, Abkar M, Moosavi M. The neuroprotective effect of bsa-based nanocurcumin against 6-ohda-induced cell death in sh-sy5y cells. Avicenna J Phytomed 2019; 9: 92-100. no DOI. ##Tatton NA. Increased caspase 3 and bax immunoreactivity accompany nuclear gapdh translocation and neuronal apoptosis in parkinson's disease. Exp neurol 2000; 166: 29-43. DOI: 10.1006/exnr.2000.7489. ##Woodgate A, MacGibbon G, Walton M, Dragunow M. The toxicity of 6-hydroxydopamine on pc12 and p19 cells. Molecular Brain Research 1999; 69: 84-92. DOI: 10.1016/s0169-328x(99)00103-5. ##Wu Y, Zhang W, Li M, Cao D, Yang X, Gong J. Nobiletin ameliorates ischemia–reperfusion injury by suppressing the function of kupffer cells after liver transplantation in rats. Biomed Pharmacother 2017; 89: 732-741. DOI: 10.1016/j.biopha.2017.02.087. ##Xie HR, Hu LS, Li GY. Sh-sy5y human neuroblastoma cell line: In vitro cell model of dopaminergic neurons in parkinson's disease. Chin Med J (Engl) 2010; 123: 1086-92. DOI: 10.3760/cma.j.issn.0366-6999.2010. 08.021. ##Xing C, Peng Y, Chang R, Yin Y, Xie Z. Effects of insulin-like growth factor-1 on okadaic acid-induced apoptosis in sh-sy5y cells. Cell Biol Int 2005; 29: 803-8. DOI: 10.1016/j.cellbi.2005.04.012. ##Yabuki Y, Ohizumi Y, Yokosuka A, Mimaki Y, Fukunaga K. Nobiletin treatment improves motor and cognitive deficits seen in mptp-induced parkinson model mice. Neuroscience 2014; 259: 126-41. DOI: 10.1016/j.neuroscience.2013.11.051. ##Yamada M, Kida K, Amutuhaire W, Ichinose F, Kaneki M. Gene disruption of caspase-3 prevents mptp-induced parkinson's disease in mice. Biochem Biophys Res Commun 2010; 402: 312-8. DOI: 10.1016/j.bbrc. 2010.10.023. ##Zhang L, Zhang X, Zhang C, Bai X, Zhang J, Zhao X, et al. Nobiletin promotes antioxidant and anti-inflammatory responses and elicits protection against ischemic stroke in vivo. Brain Res 2016; 1636: 130-41. DOI: 10.1016/j.brainres.2016.02.013. ##Zhang N, Wei W-Y, Yang Z, Che Y, Jin Y-G, Liao H-H, et al. Nobiletin, a polymethoxy flavonoid, protects against cardiac hypertrophy induced by pressure-overload via inhibition of napdh oxidases and endoplasmic reticulum stress. Cell Physiol Biochem 2017; 42: 1313-1325. DOI: 10.1159/000478960.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Combination effect of ecstasy and curcumin on hematological parameters and serum immunoglobulin levels in early and late phase in male rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Consumption of ecstasy (3,4-methylenedioxymethamphetamine, MDMA), a derivative of amphetamine, can results in various undesirable side effects including hematological and serological parameters. This study is intended to examine the effects of curcumin along with MDMA in the early and late phase of consumption on hematological parameters and serum immunoglobins (IgM, IgG and IgA) levels. Methods: We used 56 male rats that are divided into 7 groups: group1 (control), group2 (MDMA+vehicle1), group3 (curcumin), group4 (MDMA+early curcumin), group5 (MDMA+vehicle2), group6 (MDMA+late curcumin) and group7 (MDMA+early&#38;late curcumin). The groups were received MDMA (20mg/kg) orally and curcumin (20&#956;M/kg) intra-peritoneally for 2 and 4 weeks (n=8). After 24h of final dose, rats were anesthetized and blood samples were collected and used for determination of hematological parameters and IgM, IgG and IgA levels using a Coulter Automated Cell Counter and ELISA kit. Results: Our data indicated that either MDMA alone or in combination with curcumin in both early and late phases decreased lymphocytes, platelet, total leukocyte count and RBC, MCHC, RDW, immunoglobin levels, as well as hemoglobin content in comparison with the control group. In contrast, the amount of neutrophils, eosinophils, monocytes, mean cell volume and HCT increased. Furthermore, we observed blood parasites of red blood cells in the MDMA groups with curcumin. Conclusion: In conclusion, MDMA alone and in combination of curcumin altered the hematological parameters. Furthermore, their combination therapy induces toxic effects on hematological parameters and serum immunoglobin levels. This is a serious consequence for recreational drug users.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>19</FPAGE>
			<TPAGE>27</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/272019/06/102019/01/12
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1397/10/22
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/242019/10/52019/10/23
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/8/1
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Naser</Name>
				<MidName></MidName>
				<Family>Khalaji</Family>
				<NameE>Naser</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khalaji</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Adel</Name>
				<MidName></MidName>
				<Family>Mohammadzadeh</Family>
				<NameE>Adel</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mohammadzadeh</FamilyE>
				<Organizations>
				<Organization>Department of Immunology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Masoomeh</Name>
				<MidName></MidName>
				<Family>Naseri Goosheh Derag</Family>
				<NameE>Masoomeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Naseri Goosheh Derag</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Roya</Name>
				<MidName></MidName>
				<Family>Naderi</Family>
				<NameE>Roya</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Naderi</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>naderi.r@umsu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Elham</Name>
				<MidName></MidName>
				<Family>Asgari Hassanlouei</Family>
				<NameE>Elham</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Asgari Hassanlouei</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Ecstasy</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Blood cells</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Immunoglobulins</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Curcumin.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Aggarwal BB, Harikumar KB. Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases. The international journal of biochemistry &#38; cell biology 2009; 41: 40-59.##Alvarenga T, Ribeiro D, Araujo P, Hirotsu C, Mazaro-Costa R, Costa J, et al. Sleep loss and acute drug abuse can induce DNA damage in multiple organs of mice. Human &#38; experimental toxicology 2011; 30: 1275-1281.##Alvarenga TA, Andersen ML, Ribeiro DA, Araujo P, Hirotsu C, Costa JL, et al. Brief report: Single exposure to cocaine or ecstasy induces DNA damage in brain and other organs of mice. Addiction biology 2010; 15: 96-99.##Arshad L, Jantan I, Bukhari SNA, Haque MA. Immunosuppressive effects of natural α, β-unsaturated carbonyl-based compounds, and their analogs and derivatives, on immune cells: A review. Frontiers in pharmacology 2017; 8.##Boyle NT, Connor TJ. Methylenedioxymethamphetamine (‘ecstasy’)‐induced immunosuppression: A cause for concern? British journal of pharmacology 2010; 161: 17-32.##Cabral GA, Marciano-Cabral F. Cannabinoid-mediated exacerbation of brain infection by opportunistic amebae. Journal of neuroimmunology 2004; 147: 127-130.##CADET JL, JAYANTHI S, DENG X. Speed kills: Cellular and molecular bases of methamphetamine-induced nerve terminal degeneration and neuronal apoptosis. The FASEB Journal 2003; 17: 1775-1788.##Cerretani D, Riezzo I, Fiaschi AI, Centini F, Giorgi G, D’Errico S, et al. Cardiac oxidative stress determination and myocardial morphology after a single ecstasy (mdma) administration in a rat model. International journal of legal medicine 2008; 122: 461-469.##Clark A, Butt N. Ecstasy‐induced very severe aplastic anaemia complicated by invasive pulmonary mucormycosis treated with allogeneic peripheral blood progenitor cell transplant. International Journal of Laboratory Hematology 1997; 19: 279-281.##Connor TJ, Connelly DB, Kelly JP. Methylenedioxymethamphetamine (mdma;‘ecstasy’) suppresses antigen specific igg 2a and ifn-γ production. Immunology letters 2001; 78: 67-73.##Connor TJ, McNamara MG, Finn D, Currid A, O'Malley M, Redmond AM, et al. Acute 3, 4-methylenedioxymethamphetamine (mdma) administration produces a rapid and sustained suppression of immune function in the rat. Immunopharmacology 1998; 38: 253-260.##de Paula VF, Ribeiro A, Pinheiro ML, Sakai M, Lacava MC, Lapachinske SF, et al. Methylenedioxymethamphetamine (ecstasy) decreases neutrophil activity and alters leukocyte distribution in bone marrow, spleen and blood. Neuroimmunomodulation 2009; 16: 191-200.##Dhabhar FS, Miller AH, McEwen BS, Spencer RL. Effects of stress on immune cell distribution. Dynamics and hormonal mechanisms. The Journal of Immunology 1995; 154: 5511-5527.##Francis AP, Ganapathy S, Palla VR, Murthy PB, Devasena T. Future of nano bisdemethoxy curcumin analog: Guaranteeing safer intravenous delivery. Environmental toxicology and pharmacology 2015; 39: 467-474.##Friedman H, Newton C, Klein TW. Microbial infections, immunomodulation, and drugs of abuse. Clinical Microbiology Reviews 2003; 16: 209-219.##Gao S, Zhou J, Liu N, Wang L, Gao Q, Wu Y, et al. Curcumin induces m2 macrophage polarization by secretion il-4 and/or il-13. Journal of molecular and cellular cardiology 2015; 85: 131-139.##Ghosh S, Mishra R, Biswas S, Bhadra RK, Mukhopadhyay PK. Α-lipoic acid mitigates arsenic-induced hematological abnormalities in adult male rats. Iranian journal of medical sciences 2017; 42: 242.##Hall A, Henry J. Acute toxic effects of ‘ecstasy’(mdma) and related compounds: Overview of pathophysiology and clinical management. BJA: British Journal of Anaesthesia 2006; 96: 678-685.##Harms R, Morsey B, Boyer CW, Fox HS, Sarvetnick N. Methamphetamine administration targets multiple immune subsets and induces phenotypic alterations suggestive of immunosuppression. PLoS One 2012; 7: e49897.##House R, Thomas P, Bhargava H. Comparison of immune functional parameters following in vitro exposure to natural and synthetic amphetamines. Immunopharmacology and immunotoxicology 1994; 16: 1-21.##House RV, Thomas PT, Bhargava HN. Selective modulation of immune function resulting from in vitro exposure to methylenedioxymethamphetamine (ecstasy). Toxicology 1995; 96: 59-69.##Hussain Z, Thu HE, Amjad MW, Ahmed TA, Khan S. Exploring recent developments to improve antioxidant, anti-inflammatory and antimicrobial efficacy of curcumin: A review of new trends and future perspectives. Materials Science and Engineering: C 2017.##Jaehne EJ, Salem A, Irvine RJ. The effect of long-term repeated exposure to 3, 4-methylenedioxymethamphetamine on cardiovascular and thermoregulatory changes. Psychopharmacology 2008; 201: 161-170.##KankaanpÄÄ A, Meririnne E, Lillsunde P, SeppÄlÄ T. The acute effects of amphetamine derivatives on extracellular serotonin and dopamine levels in rat nucleus accumbens. Pharmacology Biochemistry and Behavior 1998; 59: 1003-1009.##Kuwayama K, Inoue H, Kanamori T, Tsujikawa K, Miyaguchi H, Iwata Y, et al. Uptake of 3, 4-methylenedioxymethamphetamine and its related compounds by a proton-coupled transport system in caco-2 cells. Biochimica et Biophysica Acta (BBA)-Biomembranes 2008; 1778: 42-50.##Lal J, Gupta S, Thavaselvam D, Agarwal D. Design, synthesis, synergistic antimicrobial activity and cytotoxicity of 4-aryl substituted 3, 4-dihydropyrimidinones of curcumin. Bioorganic &#38; medicinal chemistry letters 2012; 22: 2872-2876.##Lee JS, Bukhari SNA, Fauzi NM. Effects of chalcone derivatives on players of the immune system. Drug design, development and therapy 2015; 9: 4761.##Marsh J, Abboudi Z, Gibson F, Scopes J, Daly S, O'shaunnessy D, et al. Aplastic anaemia following exposure to 3, 4‐methylenedioxymethamphetamine (‘ecstasy’). British journal of haematology 1994; 88: 281-285.##McNamara R, Maginn M, Harkin A. Caffeine induces a profound and persistent tachycardia in response to mdma (“ecstasy”) administration. European journal of pharmacology 2007; 555: 194-198.##Mobaraki F, Seghatoleslam M, Fazel A, Ebrahimzadeh-Bideskan A. Effects of mdma (ecstasy) on apoptosis and heat shock protein (hsp70) expression in adult rat testis. Toxicology Mechanisms and Methods 2017: 1-11.##Nasir Abbas Bukhari S, G Franzblau S, Jantan I, Jasamai M. Current prospects of synthetic curcumin analogs and chalcone derivatives against mycobacterium tuberculosis. Medicinal Chemistry 2013; 9: 897-903.##Prakash UN, Srinivasan K. Fat digestion and absorption in spice‐pretreated rats. Journal of the Science of Food and Agriculture 2012; 92: 503-510.##Reichman H, Rozenberg P, Munitz A. Mouse eosinophils: Identification, isolation, and functional analysis. Current Protocols in Immunology 2017: 14.43. 1-14.43. 22.##Rigg KK, Lawental M. Perceived risk associated with mdma (ecstasy/molly) use among african americans: What prevention and treatment providers should know. Substance Use &#38; Misuse 2017: 1-8.##Rodrigues T, Reker D, Schneider P, Schneider G. Counting on natural products for drug design. Nature chemistry 2016; 8: 531-541.##Roy S, Ninkovic J, Banerjee s, Charboneau RG, Das S,Dutta R et al. Opiod drug abuse and modulation of immune function: consequences in the susceptibility to opportunistic infections. J Neuroimmune Pharmacol 2011; 6: 442-65. doi: 10.1007/s11481-011-9292-5. Epub 2011 Jul 26.##Shao M-J, Zhu Y-J, Qiu Y-E, Hu M, He Y-Q. Changes in the level of immunoglobulins and cd4/cd8 ratio in young and aged mice with estradiol deficiency. Immunological Investigations 2017; 46: 305-313.##Soetikno V, Sari FR, Veeraveedu PT, Thandavarayan RA, Harima M, Sukumaran V, et al. Curcumin ameliorates macrophage infiltration by inhibiting nf-κb activation and proinflammatory cytokines in streptozotocin induced-diabetic nephropathy. Nutrition &#38; metabolism 2011; 8: 35.##Srivastava R. Inhibition of neutrophil response by curcumin. Inflammation Research 1989; 28: 298-303.##Storka A, Vcelar B, Klickovic U, Gouya G, Weisshaar S, Aschauer S, et al. Effect of liposomal curcumin on red blood cells in vitro. Anticancer research 2013; 33: 3629-3634.##Tichelli A, Gratwohl A, Nissen C, Signer E, Gysi CS, Speck B. Morphology in patients with severe aplastic anemia treated with antilymphocyte globulin. Blood 1992; 80: 337-345.##Wu P-H, Shen Y-C, Wang Y-H, Chi C-W, Yen J-C. Baicalein attenuates methamphetamine-induced loss of dopamine transporter in mouse striatum. Toxicology 2006; 226: 238-245.##Yamamoto BK, Raudensky J. The role of oxidative stress, metabolic compromise, and inflammation in neuronal injury produced by amphetamine-related drugs of abuse. Journal of Neuroimmune Pharmacology 2008; 3: 203-217.##Young NA, Bruss MS, Gardner M, Willis WL, Mo X, Valiente GR, et al. Oral administration of nano-emulsion curcumin in mice suppresses inflammatory-induced nfκb signaling and macrophage migration. PloS one 2014; 9: e111559.##Zhou S, Yao D, Guo L, Teng L. Curcumin suppresses gastric cancer by inhibiting gastrin‐mediated acid secretion. FEBS Open Bio.##Zou J, Su C, Luo H, Lei Y, Zeng B, Zhu H, et al. Curcumin converts foxp3+ regulatory t cells to t helper 1 cells in patients with lung cancer. Journal of Cellular Biochemistry.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Prescribing patterns of antibiotics outpatients received by pharmacies in Medan city, Indonesia in 2017</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: This study aimed to determine the patterns of antibiotic use from prescriptions of physicians received by pharmacies in Medan from January to March 2017. Methods: This study was conducted in a cross-sectional method using direct observation of prescriptions received by 100 pharmacies in Medan city. The data obtained were analyzed descriptively and grouped based on the antibiotic names, antibiotic classes, type of drugs, dosage forms and prescriptions. Results: A total of 12,388 prescription sheets were obtained from 100 pharmacies in Medan during the study period in which 3,823 of the prescription sheets (30.96%) contained antibiotics. According to the data, 4,029 antibiotics were prescribed by physicians in which amoxicillin (20.63%) and cephalosporin groups (25.94%) as the most widely prescribed antibiotic and antibiotic class, respectively. A total of 1,923 antibiotics (47.73%) were prescribed with generic names and more than half of the antibiotics were prescribed in the dosage form of tablets (65.65%). This study also found that Ear Nose Throat (ENT) specialists are medical doctors who prescribe antibiotics the most. Conclusion: Based on the study results, it can be concluded that the frequency of antibiotic prescriptions is still quite high in which amoxicillin as the most commonly prescribed antibiotic. In addition, ENT specialists as the most frequent prescribers of antibiotics.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>28</FPAGE>
			<TPAGE>33</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/272019/06/102019/01/122019/03/20
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1397/12/29
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/242019/10/52019/10/232019/10/23
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/8/1
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Khairunnisa</Name>
				<MidName></MidName>
				<Family>Khairunnisa</Family>
				<NameE>Khairunnisa</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khairunnisa</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology, Faculty of Pharmacy, Universitas Sumatera Utara, Indonesia</Organization>
				</Organizations>
				<Countries>
				<Country>Indonesia</Country>
				</Countries>
				<EMAILS>
				<Email>khairunnisa7@usu.ac.id</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Embun</Name>
				<MidName></MidName>
				<Family>Suci Nasution</Family>
				<NameE>Embun</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Suci Nasution</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology, Faculty of Pharmacy, Universitas Sumatera Utara, Indonesia</Organization>
				</Organizations>
				<Countries>
				<Country>Indonesia</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Antibiotics</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Drug use patterns</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Pharmacy</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Prescription.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
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		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Sub-threshold electrical stimulation improves wingless-type3 and eukaryotic initiation factor-2α expression in the presence of exogenous astrocyte in the rat model of spinal cord injury</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Spinal cord injury (SCI) is a condition which can lead to permanent loss of neurons, glial and precursor cells. According to the positive influences of electrical stimulation in the neurogenesis, we hypothesized that sub-threshold electrical stimulation in the presence of exogenous astrocyte may trigger the differential regulation of wingless-type3 (Wnt-3) and eukaryotic initiation factor-2&#945; (eIF2&#945;) mediators in spinal cord injured rats. Methods: Forty male Wistar rats (weighing 250-280g) were randomly divided into four groups: sham, SCI, SCI+astrocyte and SCI+astrocyte which followed by electrical stimulation. We evaluated the glial fibrillary acidic protein (GFAP), doublecortin, Wnt-3 and eIF2&#945; proteins by immunofluorescence and immunoblotting techniques. Results: The results show that expression of Wnt-3 and eIF2&#945; proteins significantly enhanced after 14 days in the electrical stimulation+ SCI+astrocyte group in comparison with SCI and SCI+astrocyte groups. Also, the expression of GFAP cells was significantly increased after 14 days by electrical stimulation compared with other groups. Electrical stimulation had no effect on expression of doublecortin after 14 days. Conclusion: This survey demonstrates that sub-threshold electrical stimulation up-regulates Wnt-3 and eIF2&#945; mediators. Also, GFAP marker expression has been increased in animals subjected to electrical stimulation. But there are no evidences based on doublecortin expression as a neurogenesis biomarker.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>34</FPAGE>
			<TPAGE>45</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/272019/06/102019/01/122019/03/202019/08/17
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1398/5/26
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/242019/10/52019/10/232019/10/232019/10/23
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/8/1
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Meysam</Name>
				<MidName></MidName>
				<Family>Ghorbani</Family>
				<NameE>Meysam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ghorbani</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Parviz</Name>
				<MidName></MidName>
				<Family>Shahabi</Family>
				<NameE>Parviz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Shahabi</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>shahabip@tbzmed.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Pouran</Name>
				<MidName></MidName>
				<Family>Karimi</Family>
				<NameE>Pouran</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Karimi</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>pouran.karimi@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad</Name>
				<MidName></MidName>
				<Family>Javan</Family>
				<NameE>Mohammad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Javan</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Soheila</Name>
				<MidName></MidName>
				<Family>Bani</Family>
				<NameE>Soheila</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Bani</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Saba</Name>
				<MidName></MidName>
				<Family>Hoseini</Family>
				<NameE>Saba</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Hoseini</FamilyE>
				<Organizations>
				<Organization>Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Hamid</Name>
				<MidName></MidName>
				<Family>Soltani-Zangbar</Family>
				<NameE>Hamid</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Soltani-Zangbar</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Tabriz University of Medical Sciences, Faculty of Advanced Medical Sciences, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Behnaz</Name>
				<MidName></MidName>
				<Family>Sadeghzadeh-Oskouei</Family>
				<NameE>Behnaz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Sadeghzadeh-Oskouei</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Spinal cord injury</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Electrical stimulation</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>GFAP</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Doublecortin</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Wingless-type3.</KeyText>
			</KEYWORD>
		</KEYWORDS>

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Glia. 50, 427-434 (2005). doi: 10.1002/ glia.20207 ##Pfisterer U., Kirkeby, A., Torper, O., Wood, J., Nelander, J., Dufour, A., Björklund, A., Lindvall, O., Jakobsson, J. &#38; Parmar, M., Direct conversion of human fibroblasts to dopaminergic neurons. Proceedings of the National Academy of Sciences. 108, 10343-10348 (2011). doi: 10.1073/pnas.1105135108 ##Pilitsis J. G., Metman, L. V., Toleikis, J. R., Hughes, L. E., Sani, S. B. &#38; Bakay, R. A., Factors involved in long-term efficacy of deep brain stimulation of the thalamus for essential tremor. (2008). doi: 10.3171/jns/ 2008/109/10/0640 ##Roffé M., Hajj, G. N., Azevedo, H. F., Alves, V. S. &#38; Castilho, B. A., IMPACT is a developmentally regulated protein in neurons that opposes the eukaryotic initiation factor 2α kinase GCN2 in the modulation of neurite outgrowth. Journal of Biological Chemistry. 288, 10860-10869 (2013). doi: 10.1074/jbc.M113.461970 ##Sadighi M., Shahabi, P., Oryan, S., Pakdel, F. G., Asghari, M. &#38; Pshapour, A., Effect of low frequency electrical stimulation on spike and wave discharges of perioral somatosensory cortex in WAG/Rij rats. Pathophysiology. 20, 171-176 (2013). doi: 10.1016/j.pathophys.2013.08.006 ##Shruster A., Ben-Zur, T., Melamed, E. &#38; Offen, D., Wnt signaling enhances neurogenesis and improves neurological function after focal ischemic injury. PloS one. 7, e40843 (2012). doi: 10.1371/journal. pone.0040843 ##Sofroniew M. V., Molecular dissection of reactive astrogliosis and glial scar formation. Trends in neurosciences. 32, 638-647 (2009). doi: 10.1016/j.tins. 2009.08.002 ##Steindler D. A. &#38; Laywell, E. D., Astrocytes as stem cells: nomenclature, phenotype, and translation. Glia. 43, 62-69 (2003). doi: 10.1002/glia.10242 ##Stock G., Sturm, V., Schmitt, H. &#38; Schlör, K., The influence of chronic deep brain stimulation on excitability and morphology of the stimulated tissue. Acta neurochirurgica. 47, 123-129 (1979). doi: 10.1007/ bf01404668 ##Su Z., Niu, W., Liu, M.-L., Zou, Y. &#38; Zhang, C.-L., In vivo conversion of astrocytes to neurons in the injured adult spinal cord. Nature communications. 5, 3338 (2014a). doi: 10.1038/ncomms4338 ##Sullivan Jr W. J., Smith, A. T. &#38; Joyce, B. R., Understanding mechanisms and the role of differentiation in pathogenesis of Toxoplasma gondii: a review. Memorias do Instituto Oswaldo Cruz. 104, 155-161 (2009). doi: 10.1590/s0074-02762009000200005 ##Takahashi K., Tanabe, K., Ohnuki, M., Narita, M., Ichisaka, T., Tomoda, K. &#38; Yamanaka, S., Induction of pluripotent stem cells from adult human fibroblasts by defined factors. cell. 131, 861-872 (2007). doi: 10.1016/ j.cell.2007.11.019 ##Takahashi K. &#38; Yamanaka, S., Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. cell. 126, 663-676 (2006). doi: 10.1016/j.cell.2006.07.024 ##Thuret S., Moon, L. D. &#38; Gage, F. H., Therapeutic interventions after spinal cord injury. Nat Rev Neurosci. 7, 628-643 (2006a). doi: 10.1038/nrn1955 ##Torper O., Pfisterer, U., Wolf, D. A., Pereira, M., Lau, S., Jakobsson, J., Björklund, A., Grealish, S. &#38; Parmar, M., Generation of induced neurons via direct conversion in vivo. Proceedings of the National Academy of Sciences. 110, 7038-7043 (2013). doi: 10.1073/pnas. 1303829110 ##Valvezan A. J. &#38; Klein, P. S., GSK-3 and Wnt signaling in neurogenesis and bipolar disorder. Front Mol Neurosci. 5, (2012). doi: 10.3389/fnmol.2012.00001 ##Van Den Berge S. A., Middeldorp, J., Zhang, C. E., Curtis, M. A., Leonard, B. W., Mastroeni, D., Voorn, P., Van De Berg, W. D., Huitinga, I. &#38; Hol, E. M., Longterm quiescent cells in the aged human subventricular neurogenic system specifically express GFAP‐δ. Aging cell. 9, 313-326 (2010). doi: 10.1111/j.1474-9726. 2010.00556.x ##Vedam-Mai V., Van Battum, E., Kamphuis, W., Feenstra, M., Denys, D., Reynolds, B., Okun, M. &#38; Hol, E., Deep brain stimulation and the role of astrocytes. Molecular psychiatry. 17, 124-131 (2012). doi: 10.1038/ mp.2011.61 ##Wakabayashi T., Hidaka, R., Fujimaki, S., Asashima, M. &#38; Kuwabara, T., Diabetes Impairs Wnt3 Protein-induced Neurogenesis in Olfactory Bulbs via Glutamate Transporter 1 Inhibition. Journal of Biological Chemistry. 291, 15196-15211 (2016). doi: 10.1074/ jbc.M115.672857 ##Wang Y.-C., Peterson, S. E. &#38; Loring, J. F., Protein post-translational modifications and regulation of pluripotency in human stem cells. Cell research. 24, 143 (2014). doi: 10.1038/cr.2013.151 ##Yu Y., Tian, L., Feng, X., Cheng, J., Gong, Y., Liu, X., Zhang, Z., Yang, X., He, S., Li, C. Y. &#38; Huang, Q., eIF4E-phosphorylation-mediated Sox2 upregulation promotes pancreatic tumor cell repopulation after irradiation. Cancer Lett. 375, 31-38 (2016). doi: 10.1016/j.canlet.2016.02.052 ##Zhang X., Xin, N., Tong, L. &#38; Tong, X.-J., Electrical stimulation enhances peripheral nerve regeneration after crush injury in rats. Molecular medicine reports. 7, 1523-1527 (2013). doi: 10.3892/mmr.2013.1395## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Frankincense improves memory retrieval and down-regulates the hippocampal synaptophysin mRNA during the development of the rat brain</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Frankincense expands memory performance in different experimental models of learning. Nevertheless, the causal molecular mechanisms have not been well investigated. The expression levels of some of the synaptic proteins might probably change following the consumption of frankincense. The present study investigated the effect of maternal injection of frankincense during gestation and lactation periods on memory performance and the mRNA expression levels of syntaxin1A and synaptophysin in the hippocampus of the offspring rats. Methods: Adult female Wistar rats weighing 180-220g received two doses (50 or 100mg/kg) of the aqueous extract of frankincense by gavage during gestation and lactation periods for 45 consecutive days, except three days after labor. The control group received water. Spatial memory was assessed in the male offspring rats using the Morris water maze. Quantitative PCR was used to measure mRNAs expression levels of syntaxin1A and synaptophysin. Results: Frankincense improved spatial memory retrieval in the offspring rats. Data analysis by one-way ANOVA demonstrated that frankincense did not change the expression levels of the hippocampal syntaxin1A mRNA in the offspring rats. However, it significantly decreased the expression levels of the hippocampal synaptophysin mRNA. Conclusion: The results indicate that consumption of frankincense during both gestation and lactation periods has a beneficial impact on spatial memory performance, which is accompanied by the down-regulation of the hippocampal synaptophysin mRNA. Nevertheless, this down-regulation did not change the improving effect of frankincense in memory.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>46</FPAGE>
			<TPAGE>53</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/272019/06/102019/01/122019/03/202019/08/172019/07/17
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1398/4/26
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/242019/10/52019/10/232019/10/232019/10/232019/12/5
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/9/14
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Siamak</Name>
				<MidName></MidName>
				<Family>Beheshti</Family>
				<NameE>Siamak</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Beheshti</FamilyE>
				<Organizations>
				<Organization>Department of Plant and Animal Biology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>s.beheshti@sci.ui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Sahar</Name>
				<MidName></MidName>
				<Family>Tohidloo</Family>
				<NameE>Sahar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Tohidloo</FamilyE>
				<Organizations>
				<Organization>Department of Plant and Animal Biology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Abolghasem</Name>
				<MidName></MidName>
				<Family>Esmaeili</Family>
				<NameE>Abolghasem</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Esmaeili</FamilyE>
				<Organizations>
				<Organization>Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>aesmaeili@sci.ui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Frankincense</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Hippocampus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Spatial memory</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Synaptophysin</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Syntaxin1A.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Alder J, Xie ZP, Valtorta F, Greengard P, Poo M. Antibodies to synaptophysin interfere with transmitter secretion at neuromuscular synapses. Neuron 1992; 9: 759-68. https://doi.org/10.1016/0896-6273(92)90038-F. ##Beheshti S, Aghaie R. Therapeutic effect of frankincense in a rat model of Alzheimer's disease. Avicenna J Phytomed 2016; 6: 468-75. ##Beheshti S, Ghorbanpour Skakakomi A, Ghaedi K, Dehestani H. Frankincense upregulates the hippocampal calcium/calmodulin kinase ii-alpha during development of the rat brain and improves memory performance. Int J Dev Neurosci 2018; 69: 44-48. https://doi.org/10.1016/j.ijdevneu.2018.06.011. ##Beheshti S, Karimi B. Frankincense improves memory retrieval in rats treated with lipopolysaccharide. J HerbMed Pharmacol 2016; 5: 12-16. ##Beheshti S, Zeinali R, Esmaeili A. Rapid upregulation of the hippocampal connexins 36 and 45 mrna levels during memory consolidation. Behav Brain Res 2017; 320: 85-90. https://doi.org/10.1016/j.bbr.2016.11.048. ##Bennett MK, Garcia-Arraras JE, Elferink LA, Peterson K, Fleming AM, Hazuka CD, et al. The syntaxin family of vesicular transport receptors. Cell 1993; 74: 863-73. https://doi.org/10.1016/0092-8674(93)90466-4. ##Eastwood SL, Cairns NJ, Harrison PJ. Synaptophysin gene expression in schizophrenia. Investigation of synaptic pathology in the cerebral cortex. Br J Psychiatry 2000; 176: 236-42. https://doi.org/10.1192/bjp.176.3.236. ##Eshkind LG, Leube RE. Mice lacking synaptophysin reproduce and form typical synaptic vesicles. Cell Tissue Res 1995; 282: 423-33. https://doi.org/ 10.1007/BF00318874. ##Fujiwara T, Mishima T, Kofuji T, Chiba T, Tanaka K, Yamamoto A, et al. Analysis of knock-out mice to determine the role of hpc-1/syntaxin 1a in expressing synaptic plasticity. J Neurosci 2006; 26: 5767-76. https://doi.org/10.1523/jneurosci.0289-06.2006. ##Glantz LA, Austin MC, Lewis DA. Normal cellular levels of synaptophysin mRNA expression in the prefrontal cortex of subjects with schizophrenia. Biol Psychiatry 2000; 48: 389-97. https://doi.org/10.1016/S0006-3223(00)00923-9. ##Guo CH, Senzel A, Li K, Feng ZP. De novo protein synthesis of syntaxin-1 and dynamin-1 in long-term memory formation requires CREB1 gene transcription in lymnaea stagnalis. Behav Genet 2010; 40: 680-93. https://doi.org/10.1007/s10519-010-9374-9. ##Hosseini Sharifabad M, Esfandiary E. A morphometeric study on CA3 hippocampal field in young rats following maternal administration of boswellia serrata resin during gestation. Iran J Basic Med Sci 2007; 10: 176-182. ##Hosseini Sharifabad M, Esfandiari E. The effects of maternal administration of boswellia gum resin (frankincense) during lactation on stereological parameters of rat hippocampus. J Isfahan Med Sch 2012; 29: 2198-2207. ##Hosseini Sharifabad M, Esfandiari E, Alaei H. Effects of frankincense aqueous extract during gestational period on increasing power of learning and memory in adult offsprings. J Isfahan Med Sch 2004; 21: 16-20. ##Hosseini-Sharifabad M, Kamali-Ardakani R, Hosseini-Sharifabad A. Beneficial effect of boswellia serrata gum resin on spatial learning and the dendritic tree of dentate gyrus granule cells in aged rats. Avicenna J Phytomed 2016; 6: 189-97. ##Kwon SE, Chapman ER. Synaptophysin regulates the kinetics of synaptic vesicle endocytosis in central neurons. Neuron 2011; 70: 847-54. https://doi.org/ 10.1016/j.neuron.2011.04.001. ##Lang T, Jahn R. Core proteins of the secretory machinery. Handb Exp Pharmacol 2008: 107-27. https://doi.org/ 10.1007/978-3-540-74805-2_5. ##Liu Y, Liang Z, Liu J, Zou W, Li X, Wang Y, et al. Downregulation of caveolin-1 contributes to the synaptic plasticity deficit in the hippocampus of aged rats. Neural Regen Res 2013; 8: 2725-33. https://doi.org/10.3969/ j.issn.1673-5374.2013.29.004. ##Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative pcr and the 2(-delta delta c(t)) method. Methods 2001; 25: 402-8. https://doi.org/10.1006/meth.2001.1262. ##Lynch MA, Voss KL, Rodriguez J, Bliss TV. Increase in synaptic vesicle proteins accompanies long-term potentiation in the dentate gyrus. Neuroscience 1994; 60: 1-5. https://doi.org/10.1016/0306-4522(94)90197. ##Mahboubi M, Taghizadeh M, Talaei SA, Takht Firozeh SM, Rashidi AA, Tamtaji OR. Combined administration of Melissa officinalis and boswellia serrata extracts in an animal model of memory. Iran J Psychiatry Behav sci 2016; 10: e681. https://doi.org/10.17795/ijpbs-681. ##Mahmoudi A, Hosseini-Sharifabad A, Monsef-Esfahani HR, Yazdinejad AR, Khanavi M, Roghani A, et al. Evaluation of systemic administration of boswellia papyrifera extracts on spatial memory retention in male rats. J Nat Med 2011; 65: 519-25. https://doi.org/10.1007/s11418-011-0533-y. ##Mullany P, Lynch MA. Changes in protein synthesis and synthesis of the synaptic vesicle protein, synaptophysin, in entorhinal cortex following induction of long-term potentiation in dentate gyrus: An age-related study in the rat. Neuropharmacology 1997; 36: 973-80. https://doi.org/10.1016/s0028-3908(97)00073-7. ##Rongo C. A fresh look at the role of camkii in hippocampal synaptic plasticity and memory. Bioessays 2002; 24: 223-33. https://doi.org/10.1002/bies.10057. ##Schmitt U, Tanimoto N, Seeliger M, Schaeffel F, Leube RE. Detection of behavioral alterations and learning deficits in mice lacking synaptophysin. Neuroscience 2009; 162: 234-43. https://doi.org/10.1016/j.neuroscience. 2009.04.046. ##Shin OH. Exocytosis and synaptic vesicle function. Compr Physiol 2014; 4: 149-75. https://doi.org/10.1002/cphy. c130021. ##Singh P, Gupta A, Verma A. Herbal memory enhancer: a review. Pharma Research 2013; 10: 96-109. ##Yassin N, El-Shenawy S, Mahdy KA, Gouda N, Marrie A, Farrag A, et al. Effect of Boswellia serrata on Alzheimer’s disease induced in rats. J Arab Soc Med Res 2013; 8: 1-11.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Prenatal stress and infants’ development: association with cortisol and leptin levels in cord blood and saliva</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Stressful events during pregnancy may affect cognitive and somatic development in infants and increase the risk of developmental disorders in future. This study aimed at assessing the correlation between prenatal stress with salivary cortisol and leptin levels with a focus on infant development. Methods: In this prospective correlative study, 80 infants whose mothers were admitted to clinics during pregnancy were evaluated. The pregnant women were included during 24-28 weeks of pregnancy and assessed using the perceived stress scale until delivery. Following delivery, growth and development of infants were evaluated using the Ages and Stages Questionnaire (ASQ) at birth as well as 2, 4 and 6 months after birth. For assessing leptin and cortisol levels, cord blood and salivary samples were collected at birth and 6 months after birth, respectively. Results: The mean perceived stress score (PSS) during pregnancy was associated with infant development and weight at 2 and 6 months of age, respectively. Moreover, there was a negative association between leptin level at 6 months of age and infant height at 2, 4 and 6 months after birth. Finally, a negative correlation was observed between cortisol level at 6 months of age and infant height at 2 months following birth. Conclusion: The results indicated that the PSS of the mothers negatively correlated with the infants&#8217; growth, development and cortisol and leptin levels. Thus, prenatal stress probably affects growth and development in infancy through effects on the neuroendocrine system. Leptin might be an appropriate biomarker for determination of growth and development in infancy.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>54</FPAGE>
			<TPAGE>62</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/272019/06/102019/01/122019/03/202019/08/172019/07/172019/07/12
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1398/4/21
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/242019/10/52019/10/232019/10/232019/10/232019/12/52019/12/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/9/24
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Ehsan</Name>
				<MidName></MidName>
				<Family>Saboory</Family>
				<NameE>Ehsan</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Saboory</FamilyE>
				<Organizations>
				<Organization>Zanjan Metabolic Diseases Research Center, Zanjan University of Medical Sciences, Zanjan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>saboory@zums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Soheila</Name>
				<MidName></MidName>
				<Family>Rabiepoor</Family>
				<NameE>Soheila</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rabiepoor</FamilyE>
				<Organizations>
				<Organization>Reproductive Health Research Center, Urmia University of Medical Sciences, Urmia, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>rabieipour.s@umsu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maryam</Name>
				<MidName></MidName>
				<Family>Abedi</Family>
				<NameE>Maryam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Abedi</FamilyE>
				<Organizations>
				<Organization>Department of Midwifery, Urmia University of Medical Sciences, Urmia, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Prenatal stress</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Development</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Leptin</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Cortisol</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Saliva.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Abedi M, Sboory E, Rabiepour S, Rasouli J. The relationship between stress in pregnancy and pregnancy outcomes: A longitudinal study. J Urmia Nurs Midwifery Fac 2017; 14: 969-981. ##Adam EK, Kumari M. Assessing salivary cortisol in large-scale, epidemiological research. Psychoneuro endocrinology 2009; 34: 1423-36. DOI: 10.1016/ j.psyneuen.2009.06.011 ##Alpers GW, Abelson JL, Wilhelm FH, Roth WT. Salivary cortisol response during exposure treatment in driving phobics. Psychosom Med 2003; 65: 679-87. DOI:10.1097/01.psy.0000073872.85623.0c ##Altman D, Carroli G, Duley L, Farrell B, Moodley J, Neilson J, et al. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The magpie trial: a randomised placebo-controlled trial. Lancet 2002; 359: 1877-90. DOI:10.1016/s0140-6736(02)08778-0 ##Aschbacher K, Rodriguez-Fernandez M, van Wietmarschen H, Tomiyama AJ, Jain S, Epel E, et al. The hypothalamic-pituitary-adrenal-leptin axis and metabolic health: a systems approach to resilience, robustness and control. Interface Focus 2014; 4: 20140020. DOI: 10.1098/rsfs.2014.0020 ##Bazr Afshan M, Mahmoodi Rad A. The relationship between women's anxiety during pregnancy and labor outcomes in larestan hospitals. Mandish 2009; 1: 1-12. ##Black RE, Victora CG, Walker SP, Bhutta ZA, Christian P, de Onis M, et al. Maternal and child undernutrition and overweight in low-income and middle-income countries. Lancet 2013; 382: 427-451. DOI: 10.1016/S0140-6736(13)60937-X ##Briffa JF, McAinch AJ, Romano T, Wlodek ME, Hryciw DH. Leptin in pregnancy and development: a contributor to adulthood disease? Am J Physiol Endocrinol Metab 2015; 308: E335-50. DOI: 10.1152/ajpendo.00312.2014 ##Bronson SL, Bale TL. The placenta as a mediator of stress effects on neurodevelopmental reprogramming. Neuropsychopharmacology 2016; 41: 207-18. DOI: 10.1038/npp.2015.231 ##Cohen S, Kamarck T, Mermelstein R. A global measure of perceived stress. J Health Soc Behav 1983; 24: 385-96. DOI:http://dx.doi.org/10.13072/midss.461 ##Cookson H, Granell R, Joinson C, Ben-Shlomo Y, Henderson AJ. Mothers' anxiety during pregnancy is associated with asthma in their children. J Allergy Clin Immunol 2009; 123: 847-53. DOI: 10.1016/j.jaci. 2009.01.042 ##Ebrahimi L, Saboory E, Roshan-Milani S, Hashemi P. Effect of prenatal forced-swim stress and morphine co-administration on pentylentetrazol-induced epileptic behaviors in infant and prepubertal rats. Dev Psychobiol 2014; 56: 1179-86. DOI: 10.1002/dev.21198. Epub 2014 Jan 24 ##Eden Engstrom B, Burman P, Holdstock C, Karlsson FA. Effects of growth hormone (GH) on ghrelin, leptin, and adiponectin in GH-deficient patients. J Clin Endocrinol Metab 2003; 88: 5193-8. DOI: 10.1210/jc.2003-030713 ##Edwards HE, Dortok D, Tam J, Won D, Burnham WM. Prenatal stress alters seizure thresholds and the development of kindled seizures in infant and adult rats. Horm Behav 2002; 42: 437-47. DOI: 10.1006/ hbeh.2002.1839 ##Eftekhari MH, Ranjbar-Zahedani M, Basiratnia M, Rezaianzadeh A, Faghih S. Comparison of appetite-regulating hormones and body composition in pediatric patients in predialysis stage of chronic kidney disease and healthy control group. Iran J Med Sci 2015; 40: 27-33. ##Galic MA, Riazi K, Heida JG, Mouihate A, Fournier NM, Spencer SJ, et al. Postnatal inflammation increases seizure susceptibility in adult rats. J Neurosci 2008; 28: 6904-13. DOI: 10.1523/JNEUROSCI.1901-08.2008 ##Gat-Yablonski G, Phillip M. Leptin and regulation of linear growth. Curr Opin Clin Nutr Metab Care 2008; 11: 303-8. DOI: 10.1097/MCO.0b013e3282f795cf ##Gholipoor P, Saboory E, Ghazavi A, Kiyani A, Roshan-Milani S, Mohammadi S, et al. Prenatal stress potentiates febrile seizure and leads to long-lasting increase in cortisol blood levels in children under 2 years old. Epilepsy Behav 2017; 72: 22-27. doi: 10.1016/j.yebeh.2017.04.021 ##Gholipoor P, Saboory E, Roshan-Milani S, Fereidoni J. Effect of hyperthermia on histamine blood level and convulsive behavior in infant rats. Epilepsy Behav 2013; 29: 269-74. DOI: 10.1016/j.yebeh.2013.07.026 ##Glover V. Prenatal stress and its effects on the fetus and the child: possible underlying biological mechanisms. Adv Neurobiol 2015; 10: 269-83. DOI: 10.1007/978-1-4939-1372-5_13 ##Heshmatian B, Roshan-Milani S, Saboory E. Prenatal acute stress attenuated epileptiform activities in neonate mice. Yakhteh 2010; 12: 81-86+124. DOI: 10.22074/cellj. 2010.3778 ##Hosseini-Sharifabad M, Sabahi A. Stereological estimation of granule cell number and purkinje cell volume in the cerebellum of noise-exposed young rat. Iran J Med Sci 2014; 39: 387-90. ##Isozaki O, Tsushima T, Miyakawa M, Demura H, Seki H. Interaction between leptin and growth hormone (GH)/IGF-I axis. Endocr J 1999; 46 Suppl: S17-24. 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Acute and chronic regulation of leptin synthesis, storage, and secretion by insulin and dexamethasone in human adipose tissue. Am J Physiol Endocrinol Metab 2007; 292: E858-64. DOI: 10.1152/ajpendo.00439.2006 ##Maccari S, Darnaudery M, Morley-Fletcher S, Zuena AR, Cinque C, Van Reeth O. Prenatal stress and long-term consequences: implications of glucocorticoid hormones. Neurosci Biobehav Rev 2003; 27: 119-27. DOI:10.1016/ s0149-7634(03)00014-9 ##Nishii N, Takasu M, Ohba Y, Maeda S, Kitoh K, Ohtsuka Y, et al. Effects of administration of glucocorticoids and feeding status on plasma leptin concentrations in dogs. Am J Vet Res 2006; 67: 266-70. DOI: 10.2460/ajvr.67. 2.266 ##Oates MR. Adverse effects of maternal antenatal anxiety on children: causal effect or developmental continuum? Br J Psychiatry 2002; 180: 478-9. DOI:10.1192/bjp.180. 6.478 ##Osol G, Mandala M. Maternal uterine vascular remodeling during pregnancy. Physiology (Bethesda) 2009; 24: 58-71. 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Stress 2013; 16: 393-401. DOI: 10.3109/10253890.2013.76449## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Effects of magnesium oxide nanoparticles on memory impairment induced by postpartum depression model</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Plasma magnesium level is reduced after postpartum depression in female and this reduction can cause memory impairment. As regards the magnesium has antidepressant activity and it&#39;s deficiency leads to depression, the aim of this study was evaluating the effect of magnesium in form of magnesium oxide nanoparticles (MgO NPs) on memory retrieval in a postpartum depression model. Methods: Adult female mice (27&#177;3g) were divided into groups of control, depressed and depressed recipient of MgO NPs (1, 2.5, 5 or 10mg/kg) as an acute and chronic administrations. For induction of postpartum depression, chronic administration (5 days) of progesterone was used and three days after stopping administration, the depressive behavior was evaluated by tail suspension test. Passive avoidance memory and locomotor activity have done 24 hours after training using the step-down and open field devices, respectively. Results: Induction of postpartum depression model by the withdrawal of progesterone significantly decreased the memory retrieval. Acute administration of MgO NP significantly improved depression and memory impairment in a dose-dependent manner, while chronic administration showed less improvement in depression and memory. There was no difference between locomotor activities in all groups. Conclusion: It seems that acute administration of MgO NPs could be more suitable supplement than its chronic ones for improving depression and prevent memory impairment induced by postpartum depression. Probably the duration of nanoparticles administration can be a determining factor in their efficacy.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>63</FPAGE>
			<TPAGE>73</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/272019/06/102019/01/122019/03/202019/08/172019/07/172019/07/122019/07/18
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1398/4/27
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/242019/10/52019/10/232019/10/232019/10/232019/12/52019/12/152019/12/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/9/24
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Farzaneh</Name>
				<MidName></MidName>
				<Family>Zadehdarvish</Family>
				<NameE>Farzaneh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Zadehdarvish</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahnaz</Name>
				<MidName></MidName>
				<Family>Kesmati</Family>
				<NameE>Mahnaz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Kesmati</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>m.kesmati@scu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Lotfollah</Name>
				<MidName></MidName>
				<Family>Khajehpour</Family>
				<NameE>Lotfollah</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khajehpour</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mozhgan</Name>
				<MidName></MidName>
				<Family>Torabi</Family>
				<NameE>Mozhgan</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Torabi</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Magnesium oxide</KeyText>
			</KEYWORD>

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

			<KEYWORD>
				<KeyText>Nanoparticle</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Postpartum depression.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
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			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Prolonged hyperglycemia decreased the adverse respiratory effects of benzodiazepines in rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The incidence of diabetes is increasing along with its associated respiratory disorders, sleep disturbance and mental health problems. Despite the adverse effects of benzodiazepine receptor agonists (BZRAs) on the respiratory system function, they remain the most commonly used medications for the management of anxiety and sleep disorders. The aim of this study was to investigate whether chronic hyperglycemia increases the adverse respiratory effects of BZRAs. Methods: The experiments were carried out in male Wistar rats that were randomly allocated into six experimental groups. Hyperglycemia was induced by injecting 35mg/kg streptozotocin (STZ). We recorded breathing of conscious animals using whole-body plethysmography at the onset of the experiment and three weeks after diabetes induction. Animals were subjected to intraperitoneal injection of midazolam (0.75mg/kg) and diazepam (1mg/kg) 15min prior to the second respiratory recording. Results: Analysis of respiratory dynamics revealed an alteration in breathing pattern in intact animals following the anxiolytic dose of benzodiazepines, which was associated with an increase in respiration rate and variability and decrease in the irregularity of the respiratory rhythm. Meanwhile, these effects were significantly decreased in hyperglycemic animals. Conclusion: Our results demonstrate that STZ-induced hyperglycemic rats exhibited decreased adverse respiratory effects of BZRAs. It seems that hyperglycemia induced an impairment in benzodiazepine receptors response to the BZRAs.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>74</FPAGE>
			<TPAGE>81</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2019/03/272019/06/102019/01/122019/03/202019/08/172019/07/172019/07/122019/07/182019/09/28
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1398/7/6
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2019/08/242019/10/52019/10/232019/10/232019/10/232019/12/52019/12/152019/12/152019/12/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1398/9/24
		</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, School of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email>s.dpazhoohan@arakmu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Abbas</Name>
				<MidName></MidName>
				<Family>Alimoradian</Family>
				<NameE>Abbas</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Alimoradian</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology, School of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad</Name>
				<MidName></MidName>
				<Family>Amini</Family>
				<NameE>Mohammad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Amini</FamilyE>
				<Organizations>
				<Organization>Medical Student, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Misagh</Name>
				<MidName></MidName>
				<Family>Shafiee</Family>
				<NameE>Misagh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Shafiee</FamilyE>
				<Organizations>
				<Organization>Medical Student, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mehdi</Name>
				<MidName></MidName>
				<Family>Sadegh</Family>
				<NameE>Mehdi</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Sadegh</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School 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>Hyperglycemia</KeyText>
			</KEYWORD>

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

			<KEYWORD>
				<KeyText>Benzodiazepine</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Respiration</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Breathing pattern.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
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			</REFRENCE>
		</REFRENCES>

	</ARTICLE>

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