<?xml version="1.0" encoding="utf-8"?>
<XML>
<JOURNAL>
<YEAR>2017</YEAR>
<VOL>21</VOL>
<NO>2</NO>
<MOSALSAL>65</MOSALSAL>
<PAGE_NO>171</PAGE_NO>


<ARTICLES>

	<ARTICLE> 
		<TitleF>Actors of necroptosis scenario in cell's scene</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Necroptosis, as a novel concept, has been recently introduced in scientific literature. Much of our knowledge about necroptosis comes from ligation of tumor necrosis factor-&#945; to its receptor, TNF receptor 1. Receptor-interacting protein kinase 1, receptor-interacting protein kinase 3 and its substrate, the pseudokinase mixed lineage kinase domain-like protein, have been comprehensively studied as influential components of this process. Emerging pioneering evidence suggests that many molecules, organelles and mechanisms are involved in necroptosis pathway. The aim of this review is presentation of molecular mechanisms of necroptosis in three phases including initiation, regulation and execution of necroptosis. Moreover, this review will summarize unprecedented insights into the contribution of various organelles and cell compartments such as mitochondria, endoplasmic reticulum, nucleus, lysosomes and Golgi apparatus in necroptosis pathway.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>88</FPAGE>
			<TPAGE>101</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/12
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/9/22
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/8
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/12/18
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Sara</Name>
				<MidName></MidName>
				<Family>Nikseresht</Family>
				<NameE>Sara</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Nikseresht</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>sara.nikseresht@sbmu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Fariba</Name>
				<MidName></MidName>
				<Family>Khodagholi</Family>
				<NameE>Fariba</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khodagholi</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>khodagholi@sbmu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Abolhassan</Name>
				<MidName></MidName>
				<Family>Ahmadiani</Family>
				<NameE>Abolhassan</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ahmadiani</FamilyE>
				<Organizations>
				<Organization>Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>aahmadiani@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Cell</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Necroptosis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Organelles</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
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Brain Res 2015; 1609: 63-71.##Yoon S, Bogdanov K, Kovalenko A, Wallach D. Necroptosis is preceded by nuclear translocation of the signaling proteins that induce it. Cell Death Differ 2016; 23: 253-60.##Yu T, Sheu SS, Robotham JL, Yoon Y. Mitochondrial fission mediates high glucose-induced cell death through elevated production of reactive oxygen species. Cardiovasc Res 2008; 79: 341-51.##Yu X, Deng Q, Li W, Xiao L, Luo X, Liu X, et al. Neoalbaconol induces cell death through necroptosis by regulating ripk-dependent autocrine tnfalpha and ros production. Oncotarget 2015; 6: 1995-2008.##Zhang H, Zhong C, Shi L, Guo Y, Fan Z. Granulysin induces cathepsin b release from lysosomes of target tumor cells to attack mitochondria through processing of bid leading to necroptosis. J Immunol 2009; 182: 6993-7000.##Zhang L, Jiang F, Chen Y, Luo J, Liu S, Zhang B, et al. Necrostatin-1 attenuates ischemia injury induced cell death in rat tubular cell line nrk-52e through decreased drp1 expression. Int J Mol Sci 2013; 14: 24742-54.##Zhang M, Harashima N, Moritani T, Huang W, Harada M. The roles of ros and caspases in trail-induced apoptosis and necroptosis in human pancreatic cancer cells. PLoS One 2015; 10: e0127386.##Zhang T, Zhang Y, Cui M, Jin L, Wang Y, Lv F, et al. Camkii is a rip3 substrate mediating ischemia- and oxidative stress-induced myocardial necroptosis. Nat Med 2016; 22: 175-82.##Zhao J, Jitkaew S, Cai Z, Choksi S, Li Q, Luo J, et al. Mixed lineage kinase domain-like is a key receptor interacting protein 3 downstream component of tnf-induced necrosis. Proc Natl Acad Sci U S A 2012; 109: 5322-7.##Zhao M, Lu L, Lei S, Chai H, Wu S, Tang X, et al. Inhibition of receptor interacting protein kinases attenuates cardiomyocyte hypertrophy induced by palmitic acid. Oxid Med Cell Longev 2016; 2016: 1451676.##Zhou W, Yuan J. Necroptosis in health and diseases. Semin Cell Dev Biol 2014; 35: 14-23.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Treatment by Moringa oleifera extract can reduce gingival inflammatory cytokines in the rat periodontal model</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Overproduction of gingival pro-inflammatory cytokines have been implicated to play a noticeable role in the pathogenesis of periodontitis, which is characterized by host-mediated destruction of soft and hard periodontal tissues. Moringa oleifera (MO) is a highly valued medicinal plant which has a wide impressive range of traditional medical applications and is an alternative medicine for synthetic drugs which are accompanied with many downsides. The aim of this study was to investigate the effect of administration of the MO extract on gingival levels of TNF-&#945; and IL1-&#946; in the rat periodontal model. Methods: Inflammatory periodontitis was induced using 0-3 ligatures around the neck of right mandibular first molar in male rats. MO leaf extract was solved in dimethyl sulfoxide and injected into the gum tissue directly (500mg/kg) as a pre/post-treatment. Positive control group gave indomethacin (5mg/kg) on a daily basis. Gingival levels of TNF-&#945; and IL1-&#946; were measured using ELISA. Results: The results of this study revealed that levels of IL1-&#946; and TNF-&#945; increased in the gingival tissue in a model of periodontitis compared to control group (P&#8804;0.001). Also, the results indicated that administration of MO extract could reduce production of TNF-&#945; and IL1-&#946; in the gum tissue of rat periodontal model (P&#8804;0.001). There was no significant difference between MO extract and indomethacin anti-inflammatory effects. Conclusion: It can be concluded that pre/post-treatment with MO extract due to its direct effect on inhibition of pro-inflammatory cytokines can alleviate inflammatory symptoms in a rat periodontal model.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>102</FPAGE>
			<TPAGE>109</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/122017/01/23
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/11/4
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/82017/05/19
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1396/2/29
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mahdiyeh</Name>
				<MidName></MidName>
				<Family>Sahrakary</Family>
				<NameE>Mahdiyeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Sahrakary</FamilyE>
				<Organizations>
				<Organization>Dental Faculty, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>mahdiehsahrakari@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Vida</Name>
				<MidName></MidName>
				<Family>Nazemian</Family>
				<NameE>Vida</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Nazemian</FamilyE>
				<Organizations>
				<Organization>Neurophysiology Research Centre, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>vida.nazemian@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maryam</Name>
				<MidName></MidName>
				<Family>Aghaloo</Family>
				<NameE>Maryam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Aghaloo</FamilyE>
				<Organizations>
				<Organization>Dental Faculty, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>jzaringhalam@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Akhtar</Name>
				<MidName></MidName>
				<Family>Akbari</Family>
				<NameE>Akhtar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Akbari</FamilyE>
				<Organizations>
				<Organization>Functional Neurosurgery Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>ak_akbari86@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahdi</Name>
				<MidName></MidName>
				<Family>Shadnoush</Family>
				<NameE>Mahdi</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Shadnoush</FamilyE>
				<Organizations>
				<Organization>Faculty of Nutrition Science and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>mshadnoush@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Behzad</Name>
				<MidName></MidName>
				<Family>Nasseri</Family>
				<NameE>Behzad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Nasseri</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>nasseri.behzad@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Jalal</Name>
				<MidName></MidName>
				<Family>Zaringhalam</Family>
				<NameE>Jalal</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Zaringhalam</FamilyE>
				<Organizations>
				<Organization>Neurophysiology Research Centre, Shahid Beheshti University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>jzaringhalam@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


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

			<KEYWORD>
				<KeyText>periodontitis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>TNF-α</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>IL-1β</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Moringa Oleifera</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Aguilar-Sanchez R, Ahuatl-Garcia F, Davila-Jimenez MM, Elizalde-Gonzalez MP, Guevara-Villa MRG. Chromatographic and electrochemical determination of quercetin and kaempferol in phytopharmaceuticals. J. Pharmaceut. Biomed. Anal. 2005; 38: 239-249.##Bansal S, Rastigo S, Bajpai M, Mechanical,chemical and herbal aspects of periodontitis: a review. IJSR 5 (2012) 1260-67. ##Ezeamuzie I, Ambakederemo A, Shode F, Ekwebelem S, Antiinflammatory effects of Moringa oleifera root extract. Int J Pharmacogn 34 (1996) 207-12.##Graves DT, The potential role of chemokines and inflammatory cytokines in periodontal disease progression. Clin Infect Dis 28 (1999) 482-90. ##Guardia T, Rotelli AE, Juarez AO, Pelzer LE, Anti-inflammatory properties of plant flavonoids. Effects of rutin, quercetin and hesperidin on adjuvant arthritis in rat. Il farmaco 56 (2001) 67-83.##Gupta M, Kanti MU, Chakrabarti S, CNS activities of methanolic extract of Moringa oleifera root in mice. Fitoterapia 70 (1999) 244-50.##Hukkeri VI, Nagathan CV, Karadi RV, Patil BS, Antipyretic and wound healing activities of moringa oleifera lam. in rats. Indian J Pharm Sci 68 (2006) 124-6.##Ionel A, Lucaciu O, Moga M, Buhatel D, Ilea A, Tabaran F, et al., Periodontal disease induced in Wistar rats-experimental study. HVM Bioflux 7 (2015) 90-95.##Lampronti I, Khan MT, Borgatti M, Bianchi N, Gambari R, Inhibitory effects of Bangladeshi medicinal plant extracts on interactions between transcription factors and target DNA sequences. Evid Based Complement Alternat Med 5 (2008) 303-12.##Mahajan SG, Mali RG, Mehta AA, Protective effect of ethanolic extract of seeds of Moringa oleifera Lam. against inflammation associated with development of arthritis in rats. J Immunotoxicol 4 (2007) 39-47.##Manaheji H, Jafari S, Zaringhalam J, Rezazadeh S, Taghizadfarid R, Analgesic effects of methanolic extracts of the leaf or root of Moringa oleifera on complete Freund’s adjuvant-induced arthritis in rats. Zhong Xi Yi Jie He Xue Bao 9 (2011) 216-22.##Mohamad khani zade A, Zaringhalam Moghadam J, Sonboli A, Ayari M, Mirjafari S, Effects of hydroalcholic and chloroformic extracts of Salvia Candidissima on hyperalgesia and edema during adjuvant-induced arthritis. Koomesh 16 (2015) 239-45.##Ndiaye M, Dieye A, Mariko F, Tall A, Sall DA, Faye B, Contribution to the study of the anti-inflammatory activity of Moringa oleifera (moringaceae). Dakar Med 47 (2001) 210-12. ##Ndong M, Uehara M, Katsumata S, Sato S, Suzuki K, Preventive effects of Moringa oleifera (Lam) on hyperlipidemia and hepatocyte ultrastructural changes in iron deficient rats. Biosci Biotechnol Biochem 71 (2007) 1826-33.##Pellegrini G, Seol YJ, Gruber R, Giannobile WV, Pre-clinical models for oral and periodontal reconstructive therapies. J Dent Res 88 (2009) 1065-76.##Rizzo A, Bevilacqua N, Guida E, et al., Effect of rcsveratrol and modulation of cytokine    production on human periodontal ligament cells. Cytokine 60 (2012) 197-204. ##Ryan ME, Golub LM, Modulation of matrix metalloproteinase activities in periodontitis as a treatment strategy. Periodontol 24 (2000) 226-38.##Salvi GE, Lang NP, The effects of non-steroidal anti-inflammatory drugs (selective and non-selective) on the treatment of periodontal diseases. Curr Pharm Des 11 (2005) 1757-69.##Saliva E, Lang P, Host response modulation in the management of periodontal disease. J Clin periodontal 35 (2005) 108-29. 	##Sashidhara KV, Rosaiah JN, Tyagi E, Shukla R, Raghubir R, Rajendran SM, Rare dipeptide and urea derivatives from roots of Moringa oleifera as potential anti-inflammatory and antinociceptive agents. Eur J Med Chem 44 (2009) 432-36.##Shadnoush M, Nazemian V, Manaheji H, Zaringhalam J, Effect of probiotic administration on acute inflammatory pain. Middle East J Rehabil Health 4 (2016) 1-10.##Struillou X, Boutigny H, Soueidan A, Layrolle P, Experimental animal models in periodontology: a review. Open Dent J 4 (2010) 37-47.##Trease GE, Evans WC. Textbook of Pharmacognosy. 12th edition. London, UK: Tindall; (1983).##Vinoth B, Manivasagaperumal R, Balamurugan S, Phytochemical analysis and antibacterial activity of moringa oleifera lam. Int J Res Biol Sci 2 (2012) 98-102.##Yamaguchi M, Kasai K, Inflammation in periodontal tissue in response to mechanical forces. Arch Immunol Ther Exp 53 (2005) 388-98. ## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Effects of preconditioning with intermittent normobaric hyperoxia on TNFR1 and TNFR2 expression in the rat brain</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Recent studies have shown that intermittent normobaric hyperoxia (HO) protects the rat brain from ischemia reperfusion injury. However, the exact mechanism of this kind of protection in vivo is not known. In this study, the effect of HO on expression of TNFR1 and TNFR2 in a stroke model was investigated.&#160;Methods: In this experimental study, rats were divided into 4 groups: normoxia &#8211; sham, hyperoxia &#8211; sham, normoxia &#8211; stroke and hyperoxia &#8211;stroke for each factor (TNFR1 or TNFR2). Hyperoxia groups were exposed to 95% inspired oxygen for 4 h/day and 6 consecutive days. Oxygen concentration in the control groups was 21% (normoxia, room air). After 24h, the rats were subjected to 60 min of right middle cerebral artery occlusion (MCAO). After 24h reperfusion, neurological deficit scores (NDS) and TNFR1, 2 brain levels using Western Blot were assessed. Results: Preconditioning with HO decreased NDS. Also, followed by stroke and reperfusion, TNFR1 levels significantly increased; while there was no significant difference in hyperoxia groups compared with normoxia groups in the cortex, HO significantly reduced TNFR1 expression in subcortex. On the other hand, groups of stroke compared to sham groups significantly expressed lower levels of TNFR2 in the cortex and subcortex. There was no significant difference in hyperoxia groups compared with normoxia groups in these areas. Conclusion: Although additional studies will be required to further elucidate precise mechanisms of ischemic tolerance, it seems that HO is associated with the expression of TNFR1 in subcortex, consistent with an active role in the genesis of ischemic protection.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>110</FPAGE>
			<TPAGE>119</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/122017/01/232017/01/30
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/11/11
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/82017/05/192017/05/23
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1396/3/2
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Firoozeh</Name>
				<MidName></MidName>
				<Family>Alavian</Family>
				<NameE>Firoozeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Alavian</FamilyE>
				<Organizations>
				<Organization>Farhangian University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>f.alavian@cfu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Sohrab</Name>
				<MidName></MidName>
				<Family>Hajizadeh</Family>
				<NameE>Sohrab</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Hajizadeh</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>hajizads@modares.ac.ir</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, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>mjavan@modares.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad Reza</Name>
				<MidName></MidName>
				<Family>Bigdeli</Family>
				<NameE>Mohammad Reza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Bigdeli</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Shahid Beheshti University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>bigdelimohammadreza@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Hyperoxia</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Stroke</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>MCAO</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>TNFR1</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>TNFR2</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>1.	Ovbiagele B, Goldstein LB, Higashida RT, Howard VJ, Johnston SC, Khavjou OA, et al. Forecasting the future of stroke in the united states a policy statement from the american heart association and american stroke association. Stroke 2013; 44 (8): 2361-2375.##2.	Kitagawa K, Matsumoto M, Tagaya M, Hata R, Ueda H, Niinobe M, et al. Ischemic tolerance phenomenon found in the brain. Brain research 1990; 528 (1): 21-24.##3.	Kato H, Liu Y, Araki T, Kogure K. MK-801, but not anisomycin, inhibits the induction of tolerance to ischemia in the gerbil hippocampus. Neuroscience letters 1992; 139 (1): 118-121.##4.	Kirino T. Ischemic tolerance. Cereb Blood Flow Metab 2002; 22: 1283-1296.##5.	Chen J, Simon R. Ischemic tolerance in the brain. Neurology 1997; 48: 306-311.##6.	Perez-Pinzon MA, Mumford PL, Rosenthal M, Sick TJ. Anoxic preconditioning in hippocampal slices: role of adenosine. Neuroscience 1996; 75: 687-694.##7.	Ohtsuki T, Matsumoto M, Kuwabara K, Kitagawa K, Suzuki K, Taniguchi N, et al. Influence of oxidative stress on induced tolerance to ischemia in gerbil hippocampal neurons. Brain Res 1992; 599: 246-252.##8.	Bigdeli MR, Hajizadeha S, Froozandeh M, Rasulianc B, Heidarianpour A, Khoshbaten A. Prolonged and intermittent normobaric hyperoxia induce different degrees of ischemic tolerance in rat brain tissue. Brain Res 2007; 1152: 228-233.##9.	Wada k, Kiyazawa T, Nomura N, Yano A, Tsuzuki N, Nawashiro H, et al. Mn - SOD and Bcl-2 expression after repeated hyperbaric oxygenation. Acta Neurochir Suppl 2000; 76 (285-290).##10.	Alavian F, Hajizadeh S, Javan M, Bigdeli MR. EVALUATION OF HIF1α EXPRESSION IN ISCHEMIC TOLERANCE INDUCED BY INTERMITTENT NORMOBARIC HYPEROXIA IN THE RAT MODEL OF STROKE. 2012.##11.	Mohammadi E, Bigdeli MR. Time course of neuroprotection induced by normobaric hyperoxia and NCX1 expression. Brain injury 2014; 28 (8): 1127-1134.##12.	Alavian F, Hajizadeh S, Bigdeli MR, Bayat GR, Javan M. Evaluation of UCP2 expression in the phenomenon of ischemic resistance induced by alternating normobaric hyperoxia in a rat model of stroke. Physiology and Pharmacology 2012; 16 (1): 54-61.##13.	Bigdeli MR, Rasoulian B, Meratan AA. In vivo normobaric hyperoxia preconditioning induces different degrees of antioxidant enzymes activities in rat brain tissue. Neuropharmacology and Analgesia 2009; 611: 22–29.##14.	Liu J, Ginis I, Spatz M, Hallenbeck JM. Hypoxic preconditioning protects cultured neurons against hypoxic stress via TNF-α and ceramide. American Journal of Physiology-Cell Physiology 2000; 278 (1): C144-C153.##15.	Carswell EA, Old LJ, Kassel RL, Green S, Fiore N, Williamson B. An endotoxin-induced serum factor that causes necrosis of tumors. Proceedings of the National Academy of Sciences 1975; 72 (9): 3666-3670.##16.	Sedger LM, McDermott MF. TNF and TNF-receptors: From mediators of cell death and inflammation to therapeutic giants-past, present and future. Cytokine &#38; growth factor reviews 2014; 25 (4): 453-472.##17.	Black RA, Rauch CT, Kozlosky CJ, Peschon JJ, Slack JL, Wolfson MF, et al. A metalloproteinase disintegrin that releases tumour necrosis factor-alpha from cells. Nature 1997; 385 (6618): 729-733.##18.	Tacchini-Cottier F, Vesin C, Redard M, Buurman W, Piguet PF. Role of TNFR1 and TNFR2 in TNF-induced platelet consumption in mice. The Journal of Immunology 1998; 160 (12): 6182-6186.##19.	Yamacita-Borin FY, Zarpelon AC, Pinho-Ribeiro FA, Fattori V, Alves-Filho JC, Cunha FQ, et al. Superoxide anion-induced pain and inflammation depends on TNF/TNFR1 signaling in mice. Neuroscience letters 2015; 605: 53-58.##20.	Parameswaran N, Patial S. Tumor necrosis factor signaling in macrophages. Critical Reviewsâ„¢ in Eukaryotic Gene Expression 2010; 20 (2).##21.	Shohami E, Ginis I, Hallenbeck JM. Dual role of tumor necrosis factor alpha in brain injury. Cytokine &#38; growth factor reviews 1999; 10 (2): 119-130.##22.	Beutler B, van Huffel C. Unraveling function in the TNF ligand and receptor families. Science 1994; 264 (5159): 667-668.##23.	Aggarwal BB, Eessalu TE, Hass PE. Characterization of receptors for human tumour necrosis factor and their regulation by γ-interferon. 1985.##24.	Choi SJ, Lee K-H, Park HS, Kim S-K, Koh C-M, Park JY. Differential expression, shedding, cytokine regulation and function of TNFR1 and TNFR2 in human fetal astrocytes. Yonsei medical journal 2005; 46 (6): 818-826.##25.	Cabal-Hierro L, Noelia A, Iglesias Jn. A TRAF2 binding independent region of TNFR2 is responsibl for TRAF2 depletion and enhancement of cytotoxicity driven b TNFR1. Oncotarget 2014; 5 (1): 224.##26.	Defer N, Azroyan A, Pecker Fo, Pavoine C. TNFR1 and TNFR2 signaling interplay in cardiac myocytes. Journal of Biological Chemistry 2007; 282 (49): 35564-35573.##27.	Wan T, Xu Z, Zhou HJ, Zhang H, Luo Y, Li Y, et al. Functional Analyses of TNFR2 in Physiological and Pathological Retina AngiogenesisTNFR2 Mediates Retinal Angiogenesis. Investigative ophthalmology &#38; visual science 2013; 54 (1): 211-221.##28.	Longa EZ, Weinstein PR, Carlson S, Cummins R. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke 1989; 20: 84-91.##29.	Chen S-H, Cheung RTF. Peripheral and central administration of neuropeptide Y in a rat middle cerebral artery occlusion stroke model reduces cerebral blood flow and increases infarct volume. Brain research 2002; 927 (2): 138-143.##30.	Mohammadi E, Bigdeli MR. Effects of preconditioning with normobaric hyperoxia on Na+/Ca 2+ exchanger in the rat brain. Neuroscience 2013; 237: 277-284.##31.	Grabb M, Lobner D, Turetsky M, Choi D. Preconditioned resistance to oxygen-glucose deprivation-induced cortical neuronal death: alterations in vesicular GABA and glutamate release. Neuroscience 2002; 115: 173–183.##32.	Dittmar M, Spruss T, Schuierer G, Horn M. External carotid artery territory ischemia impairs outcome in the endovascular ﬁlament model of middle cerebral artery occlusion in rats. Stroke 2003; 34: 2252–2257.##33.	Pradillo J, Huurtado O, Romera C, Cardenas A, Fernandez P, Alonso-Escolano D, et al. TNF-R1 mediayes incereased neuronal memberane EAAT3 experession after in vivo cerebral ischemic pereconditioning. Neurosci Lett 2006; 138: 1171-1178.##34.	Romera C, Hurtado O, Botella S, Lizasoain I, Cardenas A, Fernandez-Tome P, et al. In Vitro Ischemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17–Tumor Necrosis Factor- α Pathway. J Neurosci 2004; 24: 1350 -1357.##35.	Weaver J, Liu KJ. Does normobaric hyperoxia increase oxidative stress in acute ischemic stroke? A critical review of the literature. Medical gas research 2015; 5 (1): 1.##36.	Bigdeli MR, Mohagheghi F. The Pathophysiology of Brain Ischemia and Ischemic Preconditioning. Zahedan Journal of Research in Medical Sciences 2014; 16 (2): 1-5.##37.	Bigdeli MR. Neuroprotection caused by hyperoxia preconditioning in animal stroke models. The Scientific World Journal 2011; 11: 403-421.##38.	Probert L, Akassoglou K, Pasparakis M, Kontogeorgos G, Kollias G. Spontaneous inflammatory demyelinating disease in transgenic mice showing central nervous system-specific expression of tumor necrosis factor alpha. Proceedings of the National Academy of Sciences 1995; 92 (24): 11294-11298.##39.	Yang L, Lindholm K, Konishi Y, Li R, Shen Y. Target depletion of distinct tumor necrosis factor receptor subtypes reveals hippocampal neuron death and survival through different signal transduction pathways. The Journal of neuroscience 2002; 22 (8): 3025-3032.##40.	Shen Y, Li R, Shiosaki K. Inhibition of p75 tumor necrosis factor receptor by antisense oligonucleotides increases hypoxic injury and β-amyloid toxicity in human neuronal cell line. Journal of Biological Chemistry 1997; 272 (6): 3550-3553.##41.	Marchetti L, Klein M, Schlett K, Pfizenmaier K, Eisel ULM. Tumor necrosis factor (TNF)-mediated neuroprotection against glutamate-induced excitotoxicity is enhanced by N-methyl-d-aspartate receptor activation essential role of a TNF receptor 2-mediated phosphatidylinositol 3-kinase-dependent NF-κB pathway. Journal of Biological Chemistry 2004; 279 (31): 32869-32881.##42.	Chen G, Goeddel DV. TNF-R1 signaling: a beautiful pathway. Science 2002; 296 (5573): 1634-1635.##43.	Marchetti L, Klein M, Schlett K, Pfizenmaier K, Eisel ULM. Tumor necrosis factor (TNF)-mediated neuroprotection against glutamate-induced excitotoxicity is enhanced by N-methyl-d-aspartate receptor activation essential role of a TNF receptor 2-mediated phosphatidylinositol 3-kinase-dependent NF-kB pathway. Journal of Biological Chemistry 2004; 279 (31): 32869-32881.##44.	Dong Y, Dekens DW, De Deyn PP, Naud PJW, Eisel ULM. Targeting of Tumor Necrosis Factor Alpha Receptors as a Therapeutic Strategy for Neurodegenerative Disorders. Antibodies 2015; 4 (4): 369-408.##45.	Bigdeli MR, Khoshbaten A. In vivo preconditioning with normobaric hyperoxia induces ischemic tolerance partly by triggering tumor necrosis factor-α converting enzyme/tumor necrosis factor-α/nuclear factor-κB. Neuroscience 2008; 153 (3): 671-678.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Royal jelly can modulate behavioral and histomorphometrical disorders caused by Parkinson's disease in rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The aim of present study was to investigate the effects of royal jelly (RJ) on the number of Nissl-stained neurons in caudate putamen unit (CPU) and substantia nigra pars compacta (SNC) and the thickness of gray (TGm) and white matter (TWm) of cerebral and cerebellar cortex in male rats with Parkinson&#8217;s disease (PD). Methods: Seventy five Sprague-Dawley adults&#8217; male rats were used. Rats were randomly divided into 5 groups: 1- control intact rats; 2- sham; rats received 0.02% ascorbic acid diluted in saline by CPU injection 3- PD induction without treatment; 4 and 5- PD induction + 100 or 200 mg/kg/day RJ for 21 days started 4 weeks after lesion induction. PD induction was carried out by unilateral injection of 6-hydroxydopamine in CPU. The apomorphine were done one week before lesion as well as, second, fourth and seventh weeks after lesion. Nissl-stained neurons of SNC and CPU were counted. The thickness of gray and white matter was measured by histomorphometry. Results: data showed that RJ has corrected net contralateral turns of PD. RJ at both doses significantly (P&#60;0.05) increased the number of Nissl-stained neurons in SNC and CPU in comparison to PD induction without treatment. RJ at low dose significantly (P&#60;0.05) increased TGm and TWm of the cerebral cortex and it significantly (P&#60;0.05) increased TGm but not TWm of cerebellum. RJ at high dose significantly (P&#60;0.05) increased TGm and TWm in the cerebral cortex and cerebellum. Conclusion: Results indicate that RJ can improve PD symptoms; this effect was associated with histomorphometrical disorders.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>120</FPAGE>
			<TPAGE>128</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/122017/01/232017/01/302016/11/13
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/8/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/82017/05/192017/05/232017/01/11
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/10/22
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mahnaz</Name>
				<MidName></MidName>
				<Family>Taherianfard</Family>
				<NameE>Mahnaz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Taherianfard</FamilyE>
				<Organizations>
				<Organization>Physiology Division of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>taherian2001@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Saiedeh</Name>
				<MidName></MidName>
				<Family>Ahmadi Jokani</Family>
				<NameE>Saiedeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ahmadi Jokani</FamilyE>
				<Organizations>
				<Organization>Physiology Division of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>sahmadi@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Zabihollah</Name>
				<MidName></MidName>
				<Family>Khaksar</Family>
				<NameE>Zabihollah</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khaksar</FamilyE>
				<Organizations>
				<Organization>Anatomical Division of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>khaksar@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Parkinson’s disease</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Dopamine</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Apomorphine</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Royal jelly</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Rat</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Histomorphometry</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Bohnen NI, Albin RL. White matter lesions in parkinson disease. Nat Rev Neurol 2011; 7: 229-36.##Borlongan CV, Sanberg PR. Elevated body swing test: A new behavioral parameter for rats with 6-hydroxydopamine-induced hemiparkinsonism. J Neurosci 1995; 15: 5372-8.##Choi S, Disilvio B, Fernstrom MH, Fernstrom JD. Meal ingestion, amino acids and brain neurotransmitters: Effects of dietary protein source on serotonin and catecholamine synthesis rates. Physiol Behav 2009 98: 156-62.##El-Nekeety AA, El-Kholy W, Abbas NF, Ebaid A, Amra HA, Abdel-Wahhab MA. Efficacy of royal jelly against the oxidative stress of fumonisin in rats. Toxicon 2007; 50: 256-69.##Fathy SM, abdelkader IY. Effect of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine on phosphorylated neurofilament in brain cortex of rat model for parkinson’s disease. Annual Research &#38; Review in Biology 2015; 6: 409-415.##Geday J, Ostergaard K, Johnsen E, Gjedde A. Stn-stimulation in parkinson's disease restores striatal inhibition of thalamocortical projection. Hum Brain Mapp 2009; 30: 112-21.##Gerfen CR, Surmeier DJ. Modulation of striatal projection systems by dopamine. Annu Rev Neurosci 2011; 34: 441-66.##Giompres P, Delis F. Dopamine transporters in the cerebellum of mutant mice. Cerebellum 2005; 4: 105-11.##Gonzalez-Redondo R, Garcia-Garcia D, Clavero P, Gasca-Salas C, Garcia-Eulate R, Zubieta JL, et al. Grey matter hypometabolism and atrophy in parkinson's disease with cognitive impairment: A two-step process. Brain 2014; 137: 2356-67.##Gulley RL, Wood RL. The fine structure of the neurons in the rat substantia nigra. Tissue Cell 1971; 3: 675-90.##Hashimoto M, Kanda M, Ikeno K, Hayashi Y, Nakamura T, Ogawa Y, et al. Oral administration of royal jelly facilitates mrna expression of glial cell line-derived neurotrophic factor and neurofilament h in the hippocampus of the adult mouse brain. Biosci Biotechnol Biochem 2005; 69: 800-5.##Hattori N, Nomoto H, Fukumitsu H, Mishima S, Furukawa S. Royal jelly and its unique fatty acid, 10-hydroxy-trans-2-decenoic acid, promote neurogenesis by neural stem/progenitor cells in vitro. Biomed Res 2007; 28: 261-6.##Hattori N, Nomoto H, Mishima S, Inagaki S, Goto M, Sako M, et al. Identification of amp n1-oxide in royal jelly as a component neurotrophic toward cultured rat pheochromocytoma pc12 cells. Biosci Biotechnol Biochem 2006; 70: 897-906.##Hattori N, Ohta S, Sakamoto T, Mishima S, Furukawa S. Royal jelly facilitates restoration of the cognitive ability in trimethyltin-intoxicated mice. Evid Based Complement Alternat Med 2011a; 2011: 165968.##Hattori T, Orimo S, Aoki S, Ito K, Abe O, Amano A, et al. Cognitive status correlates with white matter alteration in parkinson's disease. Hum Brain Mapp 2011b; 33: 727-39.##Hurley MJ, Mash DC, Jenner P. Markers for dopaminergic neurotransmission in the cerebellum in normal individuals and patients with parkinson's disease examined by rt-pcr. Eur J Neurosci 2003; 18: 2668-72.##Jankovic J. Parkinson's disease: Clinical features and diagnosis. J Neurol Neurosurg Psychiatry 2008; 79: 368-76.##Jia X, Lianga P, Li Y, Shi L, Wang D, Li K. Longitudinal study of gray matter changes in parkinson disease. am J Neuroradiology 2015; 36 2219-2226.##Kang DZ, Chen FY, Wang Fy, Wu GR, Liu Y, Wu G, et al. Brain gray matter volume changes associated with motor symptoms in patients with parkinson’s disease. Chinese Neurosurgical Journal 2015; 1: 9.##Lin LF, Doherty DH, Lile JD, Bektesh S, Collins F. Gdnf: A glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons. Science 1993; 260: 1130-2.##Matsuyama S, Nagao T, Sasaki K. Consumption of tyrosine in royal jelly increases brain levels of dopamine and tyramine and promotes transition from normal to reproductive workers in queenless honey bee colonies. Gen Comp Endocrinol 2015; 211: 1-8.##Melchitzky DS, Lewis DA. Tyrosine hydroxylase- and dopamine transporter-immunoreactive axons in the primate cerebellum. Evidence for a lobular- and laminar-specific dopamine innervation. Neuropsychopharmacology 2000; 22: 466-72.##Miller AE, Heyland A. Endocrine interactions between plants and animals: Implications of exogenous hormone sources for the evolution of hormone signaling. Gen Comp Endocrinol 2010; 166: 455-61.##Nagai T, Inoue R, Suzuki N, Nagashima T. Antioxidant properties of enzymatic hydrolysates from royal jelly. J Med Food 2006; 9: 363-7.##Nagai T, Nagashima T, Myoda T, Inoue R. Preparation and functional properties of extracts from bee bread. Nahrung 2004; 48: 226-9.##Olanow CW. The pathogenesis of cell death in parkinson's disease. Mov Disord 2007; 22 Suppl 17: S335-42.##Olanow CW, Agid Y, Mizuno Y, Albanese A, Bonuccelli U, Damier P, et al. Levodopa in the treatment of parkinson's disease: Current controversies. Mov Disord 2004; 19: 997-1005.##Payoux P, Remy P, Miloudi M, Houeto JL, Stadler C, Bejjani BP, et al. Contrasting changes in cortical activation induced by acute high-frequency stimulation within the globus pallidus in parkinson's disease. J Cereb Blood Flow Metab 2009; 29: 235-43.##Poewe W, Antonini A, Zijlmans JC, Burkhard PR, Vingerhoets F. Levodopa in the treatment of parkinson's disease: An old drug still going strong. Clin Interv Aging 2010; 5: 229-38.##Pyrzanowska J, Piechal A, Blecharz-Klin K, Joniec-Maciejak I, Graikou K, Chinou I, et al. Long-term administration of greek royal jelly improves spatial memory and influences the concentration of brain neurotransmitters in naturally aged wistar male rats. J Ethnopharmacol 2014; 155: 343-51.##Ribeiro MJ, Vidailhet M, Loc'h C, Dupel C, Nguyen JP, Ponchant M, et al. Dopaminergic function and dopamine transporter binding assessed with positron emission tomography in parkinson disease. Arch Neurol 2002; 59: 580-6.##Rolland AS, Herrero MT, Garcia-Martinez V, Ruberg M, Hirsch EC, Francois C. Metabolic activity of cerebellar and basal ganglia-thalamic neurons is reduced in parkinsonism. Brain 2007; 130: 265-75.##Sasaki K. Nutrition and dopamine: An intake of tyrosine in royal jelly can affect the brain levels of dopamine in male honeybees (apis mellifera l.). J Insect Physiol 2016; 87: 45-52.##Sasakia K, Matsuyamaa S, Haranob K, Nagaoa T. Caste differences in dopamine-related substances and dopamine supply in the brains of honeybees (apis mellifera l.). General and Comparative Endocrinology 2012; 178: 46–53.##Scatton B, Rouquier L, Javoy-Agid F, Agid Y. Dopamine deficiency in the cerebral cortex in parkinson disease. Neurology 1982; 32: 1039-40.##Schwarting RK, Huston JP. The unilateral 6-hydroxydopamine lesion model in behavioral brain research. Analysis of functional deficits, recovery and treatments. Prog Neurobiol 1996; 50: 275-331.##Simuth J, Bilikova K, Kovacova E, Kuzmova Z, Schroder W. Immunochemical approach to detection of adulteration in honey: Physiologically active royal jelly protein stimulating tnf-alpha release is a regular component of honey. J Agric Food Chem 2004; 52: 2154-8.##Yager LM, Garcia AF, Wunsch AM, Ferguson SM. The ins and outs of the striatum: Role in drug addiction. Neuroscience 2015; 301: 529-41.##Yoshikawa K, Nakata Y, Yamada K, Nakagawa M. Early pathological changes in the parkinsonian brain demonstrated by diffusion tensor mri. J Neurol Neurosurg Psychiatry 2004; 75: 481-4.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Alteration of OGG1, MYH and MTH1 genes expression in relapsing-remitting multiple sclerosis patients</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Previous studies revealed that oxidative stress is elevated in multiple sclerosis (MS). It can harm to biological macromolecules such as DNA. However, the molecular mechanism in protection of genetic information from DNA damages is not clear in MS disease. In this study the expression level of some important genes of OGG1 and MYH involved in base excision repair pathway and, MTH1 and ITPA as main cleaning genes of nucleotide pool from rough nucleotides are examined in MS patients in compared to healthy group. Methods: Peripheral blood mononuclear cells were isolated from relapsing-remitting-MS patients and healthy subjects. After RNA extraction and cDNA synthesis, the expression levels of target genes were examined by RT-qPCR technique. Results: The level of the MTH1 and MYH genes expression were decreased, but the level of OGG1 mRNA was higher in patients in comparison to the control group. Obtained result did not shown any correlation between expression of examined genes and clinical features of patients such as MS severity and disease duration. Conclusion: These preliminary results provide more supportive evidences for involvement of oxidative damage and variation in expression of DNA repair genes in MS. Significant increase of OGG1 suggest that the development and progression of pathogenesis in Iranian MS can be related to chronic and direct oxidative damage of genomic DNA not nucleotide pools.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>129</FPAGE>
			<TPAGE>136</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/122017/01/232017/01/302016/11/132017/01/27
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/11/8
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/82017/05/192017/05/232017/01/112017/05/23
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1396/3/2
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Roya</Name>
				<MidName></MidName>
				<Family>Amirinejad</Family>
				<NameE>Roya</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Amirinejad</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>amirinejad87@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad Ali</Name>
				<MidName></MidName>
				<Family>Sahraian</Family>
				<NameE>Mohammad Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Sahraian</FamilyE>
				<Organizations>
				<Organization>MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>msahrai@sina.tums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Bahram</Name>
				<MidName></MidName>
				<Family>Mohammad Soltani</Family>
				<NameE>Bahram</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mohammad Soltani</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>soltanib@modares.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mehrdad</Name>
				<MidName></MidName>
				<Family>Behmanesh</Family>
				<NameE>Mehrdad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Behmanesh</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>behmanesh@modares.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Multiple Sclerosis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>DNA repair</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Genes expression</KeyText>
			</KEYWORD>

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

			<KEYWORD>
				<KeyText>OGG1</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Adamczyk B, Adamczyk-Sowa M. New Insights into the Role of Oxidative Stress Mechanisms in the Pathophysiology and Treatment of Multiple Sclerosis. Oxidative Medicine and Cellular Longevity. 2016;2016.##Ahmadi A, Behmanesh M, Boroumand MA, Tavallaei M. Up-regulation of MSH2, XRCC1 and ATM genes in patients with type 2 diabetes and coronary artery disease. Diabetes research and clinical practice. 2015;109:500-506.##Behmanesh M,Sakumi K, Tsuchimoto D, Torisu K, Ohnishi-Honda Y, Rancourt D, Nakabeppu Y. Characterization of the Structure and Expression of Mouse Itpa Gene and its Related Sequences in the Mouse Genome. DNA Research 2005; 12:39-51.##Briggs FB, Goldstein BA, McCauley JL, Zuvich RL, De Jager PL, Rioux JD, et al. Variation within DNA      repair pathway genes and risk of multiple sclerosis. American journal of epidemiology 2010; 172:217-224.##Chen M, Carass A, Oh J, Nair G, Pham DL, Reich DS, et al. Automatic magnetic resonance spinal cord segmentation with topology constraints for variable fields of view. Neuroimage2013; 83:1051-1062.##Colton C, Gilbert D. Microglia, an in vivo source of reactive oxygen species in the brain. Advances in neurology1993;59:321-326.##Eshtad S, Mavajian Z, Rudd S, Visnes T, Boström J, Altun M, et al. hMYH and hMTH1 cooperate for survival in mismatch repair defective T-cell acute lymphoblastic leukemia. Oncogenesis 2016;5:e275.##Gon S, Napolitano R, Rocha W, Coulon S, Fuchs RP. Increase in dNTP pool size during the DNA damage response plays a key role in spontaneous and induced-mutagenesis in Escherichia coli. Proceedings of the National Academy of Sciences 2011;108:19311-19316.##Grecchi S, Mazzini G, Lisa A, Armentero M-T, Bergamaschi R, Romani A, et al. Search for cellular stress biomarkers in lymphocytes from patients with multiple sclerosis: a pilot study. PloS one 2012;7(9):e44935.##Haider L, Fischer MT, Frischer JM, Bauer J, Höftberger R, Botond G, et al. Oxidative damage in multiple sclerosis lesions. Brain 2011;awr128.##Ibitoye R, Kemp K, Rice C, Hares K, Scolding N, Wilkins A. Oxidative stress-related biomarkers in multiple sclerosis: a review. Biomarkers in Medicine 2016;10:889-902.##Nakabeppu Y. Cellular levels of 8-oxoguanine in either DNA or the nucleotide pool play pivotal roles in carcinogenesis and survival of cancer cells. International journal of molecular sciences. 2014;15:12543-12557.##Karahalil B, Orhan G, Ak F. The impact of detoxifying and repair gene polymorphisms and the levels of serum ROS in the susceptibility to multiple sclerosis. Clinical neurology and neurosurgery 2015;139:288-294.##Kremer TM, Rinne ML, Xu Y, Chen XM, Kelley MR. Protection of pulmonary epithelial cells from oxidative stress by hMYH adenine glycosylase. Respiratory research 2004;5:1.##Livak K.J., Schmittgen T.D., Analysis of relative gene expression data using real-time quantitative PCR and the 2(−delta delta C (T)) method, Methods2001; 25 :402–408.##Ljubisavljevic S, Stojanovic I, Basic J, Pavlovic D. The Validation Study of Neurofilament Heavy Chain and 8-hydroxy-2′-deoxyguanosine as Plasma Biomarkers of Clinical/Paraclinical Activity in First and Relapsing-Remitting Demyelination Acute Attacks. Neurotoxicity research.2016;30:530-538.##McDonald WI, Compston A, Edan G, Goodkin D, Hartung H-P, Lublin FD, et al. Recommended diagnostic criteria for multiple sclerosis: guidelines from the international panel on the diagnosis of multiple sclerosis. Ann Neurol 2001;50:121–127.##Mandel M, Gurevich M, Pauzner R, Kaminski N, Achiron A. Autoimmunity gene expression portrait: specific signature that intersects or differentiates between multiple sclerosis and systemic lupus erythematosus. Clinical &#38; Experimental Immunology 2004;138:164-170.##Miljković D, Spasojević I. Multiple sclerosis: molecular mechanisms and therapeutic opportunities. Antioxidants &#38; redox signaling 2013;19:2286-2334.##Miller E, Mrowicka M, Saluk-Juszczak J, Ireneusz M. The level of isoprostanes as a non-invasive marker for in vivo lipid peroxidation in secondary progressive multiple sclerosis. Neurochemical research 2011;36:1012-1016.##Nakauchi A, Wong JH, Mahasirimongkol S, Yanai H, Yuliwulandari R, Mabuchi A, et al. Identification of ITPA on chromosome 20 as a susceptibility gene for young-onset tuberculosis. Human genome variation 2016;3:15067.##Naghavi Gargari B., Behmanesh M., Sahraian M.A., Effect of vitamin D treatment on interleukin-2 and interleukin-4 genes expression in multiple sclerosis. Physiol.Pharmacol 2015;19 : 14–21.##Nunomura A, Moreira P, Takeda A, Smith M, Perry G. Oxidative RNA damage and neurodegeneration. Current medicinal chemistry 2007;14:2968-2975.##Ohl K, Tenbrock K, Kipp M. Oxidative stress in multiple sclerosis: Central and peripheral mode of action. Experimental neurology 2016;277:58-67.##Papeo G. MutT Homolog 1 (MTH1): The Silencing of a Target. Journal of medicinal chemistry 2016;59:2343-2345.##Peterson JR, Thor S, Kohler L, Kohler PR, Metcalf WW, Luthey-Schulten Z. Genome-wide gene expression and RNA half-life measurements allow predictions of regulation and metabolic behavior in Methanosarcina acetivorans. BMC genomics. 2016;17:924.##Polachini CRN, Spanevello RM, Zanini D, Baldissarelli J, Pereira LB, Schetinger MRC, et al. Evaluation of Delta-Aminolevulinic Dehydratase Activity, Oxidative Stress Biomarkers, and Vitamin D Levels in Patients with Multiple Sclerosis. Neurotoxicity research 2016;29:230-242.##Prieto A, Díaz D, Barcenilla H, Castrillo C, Monserrat J, Merino AG, et al. Increased spontaneous ex vivo apoptosis and subset alterations in peripheral blood T cells from patients with multiple sclerosis. Journal of clinical immunology 2006;26:101-112.##Satoh J-i, Nakanishi M, Koike F, Miyake S, Yamamoto T, Kawai M, et al. Microarray analysis identifies an aberrant expression of apoptosis and DNA damage-regulatory genes in multiple sclerosis. Neurobiology of disease2005;18:537-550.##Selvaraj V, Soundarapandian MM, Chechneva O, Williams AJ, Sidorov MK, Soulika AM, et al. PARP-1 deficiency increases the severity of disease in a mouse model of multiple sclerosis. Journal of Biological Chemistry 2009;284:26070-26084.##Sliwinska A, Kwiatkowski D, Czarny P, Toma M, Wigner P, Drzewoski J, et al. The levels of 7, 8-dihydrodeoxyguanosine (8-oxoG) and 8-oxoguanine DNA glycosylase 1 (OGG1)–A potential diagnostic biomarkers of Alzheimer's disease. Journal of the Neurological Sciences 2016;368:155-159.##Tajouri L, Mellick AS, Ashton KJ, Tannenberg AE, Nagra RM, Tourtellotte WW, et al. Quantitative and qualitative changes in gene expression patterns characterize the activity of plaques in multiple sclerosis. Molecular brain research 2003;119:170-183.##Tasset I, Agüera E, Sánchez-López F, Feijóo M, Giraldo AI, Cruz AH, et al. Peripheral oxidative stress in relapsing–remitting multiple sclerosis. Clinical biochemistry 2012;45:440-444.##Villoslada P. Neuroprotective therapies for multiple sclerosis and other demyelinating diseases. Multiple Sclerosis and Demyelinating Disorders 2016;1:1.##Zhang Q, Fujino M, Xu J, Li X-k. The role and potential therapeutic application of myeloid-derived suppressor cells in allo-and autoimmunity. Mediators of inflammation2015;2015:#### ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Effects of amitriptyline and fluoxetine on synaptic plasticity and TNF-α level at hippocampus of streptozotocin-induced diabetic rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Studies have indicated that diabetes mellitus impairs hippocampus. Diabetes increases the risk of depression and treatment with antidepressants may affect learning and memory. The aim of this study was to evaluate the effects of amitriptyline and fluoxetine on synaptic plasticity and TNF-&#945; level in the hippocampus of streptozotocin-induced diabetic rats. Methods: Experimental groups were control, diabetes, diabetes-amitriptyline and diabetes-fluoxetine (n=8 for each experimental group). Three weeks after the induction of diabetes, the rats received treatment with amitriptyline (5 mg/kg) or fluoxetine (5 mg/kg) for 21 days. Long-term potentiation (LTP) in perforant path-dentate gyrus synapses was assessed (by 400 Hz tetanization) for investigating the effect of treatments on synaptic plasticity. Field excitatory post-synaptic potential indices were measured. Finally, TNF-&#945; levels were measured in hippocampus by enzyme-linked immunosorbant assay. Results: Six weeks after the diabetes induction, LTP wasn&#8217;t different between the control and the diabetes groups and also no significant differences were observed between the diabetes and the diabetes-treated groups; however, amitriptyline and fluoxetine impaired LTP in diabetic rats and there was a significant difference between the control and the diabetes-treated groups. Comparing to the controls, TNF-&#945; level was increased significantly (P&#60;0.05) only in the diabetes-amitriptyline group. Conclusion: Results suggest that amitriptyline and fluoxetine intensify the destructive effects of diabetes on hippocampus and that TNF-&#945; may act as a mediator for these changes; however, other factors may also be involved. Hence, treatment of diabetic patients with antidepressants must be done with extra care.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>137</FPAGE>
			<TPAGE>146</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/122017/01/232017/01/302016/11/132017/01/272016/10/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/8/8
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/82017/05/192017/05/232017/01/112017/05/232017/03/17
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/12/27
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Parham</Name>
				<MidName></MidName>
				<Family>Reisi</Family>
				<NameE>Parham</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Reisi</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>p_reisi@med.mui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Fatemeh</Name>
				<MidName></MidName>
				<Family>Sepahvand</Family>
				<NameE>Fatemeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Sepahvand</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>fatemeh.sepahvand75@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ghasem</Name>
				<MidName></MidName>
				<Family>Zarei</Family>
				<NameE>Ghasem</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Zarei</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>yamahdi123@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Leila</Name>
				<MidName></MidName>
				<Family>Kamali Dolatabadi</Family>
				<NameE>Leila</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Kamali Dolatabadi</FamilyE>
				<Organizations>
				<Organization>Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>leili_kamali@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Shaghayegh</Name>
				<MidName></MidName>
				<Family>Haghjooye Javanmard</Family>
				<NameE>Shaghayegh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Haghjooye Javanmard</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>shaghayegh.haghjoo@gmail.com</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></Country>
				</Countries>
				<EMAILS>
				<Email>alaei@med.mui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Amitriptyline</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Fluoxetine</KeyText>
			</KEYWORD>

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

			<KEYWORD>
				<KeyText>LTP</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>TNF-α</KeyText>
			</KEYWORD>

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

		<REFRENCES>
			<REFRENCE>
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Diabetes 1996; 45: 1259-66.##Bliss TV, Collingridge GL. A synaptic model of memory: Long-term potentiation in the hippocampus. Nature 1993; 361: 31-9.##Brunnauer A, Laux G, Geiger E, Soyka M, Moller HJ. Antidepressants and driving ability: Results from a clinical study. J Clin Psychiatry 2006; 67: 1776-81.##Caiati MD, Cherubini E. Fluoxetine impairs gabaergic signaling in hippocampal slices from neonatal rats. Front Cell Neurosci 2013; 7: 63.##Campbell S, Macqueen G. The role of the hippocampus in the pathophysiology of major depression. J Psychiatry Neurosci 2004; 29: 417-26.##Campelo SR, da Silva MB, Vieira JL, da Silva JP, Salgado CG. Effects of immunomodulatory drugs on tnf-alpha and il-12 production by purified epidermal langerhans cells and peritoneal macrophages. BMC Res Notes 2011; 4: 24.##Chadwick W, Wilson G, van de Venter M, Oelofsen W, Roux S. Shifts in metabolic parameters surrounding glucose homoeostasis resulting from tricyclic antidepressant therapy: Implications of insulin resistance? J Pharm Pharmacol 2007; 59: 95-103.##Chee J, Angstetra E, Mariana L, Graham KL, Carrington EM, Bluethmann H, et al. Tnf receptor 1 deficiency increases regulatory t cell function in nonobese diabetic mice. J Immunol 2011; 187: 1702-12.##Christen U, Wolfe T, Mohrle U, Hughes AC, Rodrigo E, Green EA, et al. A dual role for tnf-alpha in type 1 diabetes: Islet-specific expression abrogates the ongoing autoimmune process when induced late but not early during pathogenesis. J Immunol 2001; 166: 7023-32.##Cumiskey D, Butler MP, Moynagh PN, O'Connor J J. Evidence for a role for the group i metabotropic glutamate receptor in the inhibitory effect of tumor necrosis factor-alpha on long-term potentiation. Brain Res 2007; 1136: 13-9.##Curran B, O'Connor JJ. The pro-inflammatory cytokine interleukin-18 impairs long-term potentiation and nmda receptor-mediated transmission in the rat hippocampus in vitro. Neuroscience 2001; 108: 83-90.##Djordjevic A, Djordjevic J, Elakovic I, Adzic M, Matic G, Radojcic MB. Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. Eur J Pharmacol 2012; 693: 37-44.##Duarte JM. Metabolic alterations associated to brain dysfunction in diabetes. Aging Dis 2015; 6: 304-21.##Duman RS, Malberg J, Thome J. Neural plasticity to stress and antidepressant treatment. Biol Psychiatry 1999; 46: 1181-91.##Duseja R, Heir R, Lewitus GM, Altimimi HF, Stellwagen D. Astrocytic tnfalpha regulates the behavioral response to antidepressants. Brain Behav Immun 2015; 44: 187-94.##Gaspar JM, Baptista FI, Macedo MP, Ambrosio AF. Inside the diabetic brain: Role of different players involved in cognitive decline. ACS Chem Neurosci 2016; 7: 131-42.##Getz A, Xu F, Zaidi W, Syed NI. The antidepressant fluoxetine but not citalopram suppresses synapse formation and synaptic transmission between lymnaea neurons by perturbing presynaptic and postsynaptic machinery. Eur J Neurosci 2011; 34: 221-34.##Gomez R, Huber J, Tombini G, Barros HM. Acute effect of different antidepressants on glycemia in diabetic and non-diabetic rats. Braz J Med Biol Res 2001; 34: 57-64.##Habib M, Shaker S, El-Gayar N, Aboul-Fotouh S. The effects of antidepressants &#34;fluoxetine and imipramine&#34; on vascular abnormalities and toll like receptor-4 expression in diabetic and non-diabetic rats exposed to chronic stress. PLoS One 2015; 10: e0120559.##Hinze-Selch D, Schuld A, Kraus T, Kuhn M, Uhr M, Haack M, et al. Effects of antidepressants on weight and on the plasma levels of leptin, tnf-alpha and soluble tnf receptors: A longitudinal study in patients treated with amitriptyline or paroxetine. Neuropsychopharmacology 2000; 23: 13-9.##Ho N, Sommers MS, Lucki I. Effects of diabetes on hippocampal neurogenesis: Links to cognition and depression. Neurosci Biobehav Rev 2013; 37: 1346-62.##Kahya MC, Naziroglu M, Ovey IS. Modulation of diabetes-induced oxidative stress, apoptosis, and ca2+ entry through trpm2 and trpv1 channels in dorsal root ganglion and hippocampus of diabetic rats by melatonin and selenium. Mol Neurobiol 2016.##Kamal A, Biessels GJ, Duis SE, Gispen WH. Learning and hippocampal synaptic plasticity in streptozotocin-diabetic rats: Interaction of diabetes and ageing. Diabetologia 2000; 43: 500-6.##Kamal A, Biessels GJ, Urban IJ, Gispen WH. Hippocampal synaptic plasticity in streptozotocin-diabetic rats: Impairment of long-term potentiation and facilitation of long-term depression. Neuroscience 1999; 90: 737-45.##Khundakar AA, Zetterstrom TS. Biphasic change in bdnf gene expression following antidepressant drug treatment explained by differential transcript regulation. Brain Res 2006; 1106: 12-20.##Kodl CT, Seaquist ER. Cognitive dysfunction and diabetes mellitus. Endocr Rev 2008; 29: 494-511.##Kostadinov I, Delev D, Petrova A, Stanimirova I, Draganova K, Kostadinova I, et al. Study on anti-inflammatory and immunomodulatory effects of clomipramine in carrageenan- and lipopolysaccharide-induced rat models of inflammation. Biotechnol Biotechnol Equip 2014; 28: 552-558.##Laake JP, Stahl D, Amiel SA, Petrak F, Sherwood RA, Pickup JC, et al. The association between depressive symptoms and systemic inflammation in people with type 2 diabetes: Findings from the south london diabetes study. Diabetes Care 2014; 37: 2186-92.##Lee MY, Hong S, Kim N, Shin KS, Kang SJ. Tricyclic antidepressants amitriptyline and desipramine induced neurotoxicity associated with parkinson's disease. Mol Cells 2015; 38: 734-40.##Liamis G, Liberopoulos E, Barkas F, Elisaf M. Diabetes mellitus and electrolyte disorders. World Journal of Clinical Cases: WJCC 2014; 2: 488.##Loane DJ, Byrnes KR. Role of microglia in neurotrauma. Neurotherapeutics 2010; 7: 366-77.##Mahmood D, Akhtar M, Vohora D, Khanam R. Comparison of antinociceptive and antidiabetic effects of sertraline and amitriptyline on streptozotocin-induced diabetic rats. Hum Exp Toxicol 2010; 29: 881-6.##Malberg JE, Eisch AJ, Nestler EJ, Duman RS. Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus. J Neurosci 2000; 20: 9104-10.##McAfoose J, Baune BT. Evidence for a cytokine model of cognitive function. Neurosci Biobehav Rev 2009; 33: 355-66.##Miyata S, Hirano S, Kamei J. Diabetes attenuates the antidepressant-like effect mediated by the activation of 5-ht1a receptor in the mouse tail suspension test. Neuropsychopharmacology 2004; 29: 461-9.##Paxinos G, Watson, C. The rat brain in stereotaxic##coordinates, fifth ed. Academic Press,San Diego 2005; p. 387.##Reisi P, Alaei H, Babri S, Sharifi MR, Mohaddes G. Effects of treadmill running on spatial learning and memory in streptozotocin-induced diabetic rats. Neurosci Lett 2009a; 455: 79-83.##Reisi P, Alaei H, Babri S, Sharifi MR, Mohaddes G, Soleimannejad E. Determination of the extracellular basal levels of glutamate and gaba at dentate gyrus of streptozotocin-induced diabetic rats. Pathophysiology 2009b; 16: 63-6.##Reisi P, Alaei H, Babri S, Sharifi MR, Mohaddes G, Soleimannejad E, et al. Effects of treadmill running on extracellular basal levels of glutamate and gaba at dentate gyrus of streptozotocin-induced diabetic rats. Journal of Research in Medical Sciences 2010a; 15: 172-174.##Reisi P, Babri S, Alaei H, Sharifi MR, Mohaddes G, Lashgari R. Effects of treadmill running on short-term pre-synaptic plasticity at dentate gyrus of streptozotocin-induced diabetic rats. Brain Res 2008; 1211: 30-6.##Reisi P, Babri S, Alaei H, Sharifi MR, Mohaddes G, Noorbakhsh SM, et al. Treadmill running improves long-term potentiation (ltp) defects in streptozotocin-induced diabetes at dentate gyrus in rats. Pathophysiology 2010b; 17: 33-8.##Renauld AE, Ignatowski TA, Spengler RN. Alpha 2-adrenergic receptor inhibition of camp accumulation is transformed to facilitation by tumor necrosis factor-alpha. Brain Res 2004; 1004: 212-6.##Reynolds JL, Ignatowski TA, Gallant S, Spengler RN. Amitriptyline administration transforms tumor necrosis factor-alpha regulation of norepinephrine release in the brain. Brain Res 2004; 1023: 112-20.##Sapolsky RM. Depression, antidepressants, and the shrinking hippocampus. Proc Natl Acad Sci U S A 2001; 98: 12320-2.##Sasaki-Hamada S, Sacai H, Oka JI. Diabetes onset influences hippocampal synaptic plasticity in streptozotocin-treated rats. Neuroscience 2012; 227: 293-304.##Strachan J, Shepherd J. Hyponatraemia associated with the use of selective serotonin re-uptake inhibitors. Aust N Z J Psychiatry 1998; 32: 295-8.##Wall AM, Mukandala G, Greig NH, O'Connor JJ. Tumor necrosis factor-alpha potentiates long-term potentiation in the rat dentate gyrus after acute hypoxia. J Neurosci Res 2015; 93: 815-29.##Wang JW, David DJ, Monckton JE, Battaglia F, Hen R. Chronic fluoxetine stimulates maturation and synaptic plasticity of adult-born hippocampal granule cells. J Neurosci 2008; 28: 1374-84.##Warner-Schmidt JL, Vanover KE, Chen EY, Marshall JJ, Greengard P. Antidepressant effects of selective serotonin reuptake inhibitors (ssris) are attenuated by antiinflammatory drugs in mice and humans. Proc Natl Acad Sci U S A 2011; 108: 9262-7.##Xu F, Luk C, Richard MP, Zaidi W, Farkas S, Getz A, et al. Antidepressant fluoxetine suppresses neuronal growth from both vertebrate and invertebrate neurons and perturbs synapse formation between lymnaea neurons. Eur J Neurosci 2010; 31: 994-1005.##Xu H, Steven Richardson J, Li XM. Dose-related effects of chronic antidepressants on neuroprotective proteins bdnf, bcl-2 and cu/zn-sod in rat hippocampus. Neuropsychopharmacology 2003; 28: 53-62.##Yau JL, Noble J, Hibberd C, Rowe WB, Meaney MJ, Morris RG, et al. Chronic treatment with the antidepressant amitriptyline prevents impairments in water maze learning in aging rats. J Neurosci 2002; 22: 1436-42.##Zarei G, Reisi P, Alaei H, Javanmard SH. Effects of amitriptyline and fluoxetine on synaptic plasticity in the dentate gyrus of hippocampal formation in rats. Adv Biomed Res 2014; 3: 199.##Zhang WJ, Tan YF, Yue JT, Vranic M, Wojtowicz JM. Impairment of hippocampal neurogenesis in streptozotocin-treated diabetic rats. Acta Neurol Scand 2008; 117: 205-10.##Zschocke J, Zimmermann N, Berning B, Ganal V, Holsboer F, Rein T. Antidepressant drugs diversely affect autophagy pathways in astrocytes and neurons--dissociation from cholesterol homeostasis. Neuropsychopharmacology 2011; 36: 1754-68.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Role of the AMPA receptors of paragigantocellularis lateralis nucleus in the inflammatory pain modulation in male rat</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The 17&#946;-estradiol acts as a neurosteroid in the brain and modulates nociception by binding to the estrogen receptors and also by allosteric interaction with other membrane-bound receptors like glutamate receptors. Paragigantocellularis lateralis nucleus (LPGi) is one of the important brain regions implicated in the pain modulation. So, this study was designed to evaluate the possible involvement of the membrane-bound AMPA receptors of LPGi nucleus in the pain modulatory effect of intra-LPGi 17&#946;-estradiol in the male rats. Methods: In order to study the pain modulatory effect of intra-LPGi microinjection of 17&#946;-estradiol, cannulation into the LPGi nucleus was performed. Then, 500 nl of saline, 17&#946;-estradiol and CNQX- the AMPA receptor antagonist- were unilaterally administered into the right LPGi by injection cannula and Hamilton syringe. In addition, for assessing the role of the AMPA receptors in the pain modulation by 17&#946;-estradiol, 17&#946;-estradiol was injected 15 min after the intra-LPGi administration of CNQX. Then, 50 &#956;l of 4% formalin was subcutaneously injected into the plantar surface of contralateral hind paw and the number of paw jerking behavior was observed for 60 min. Results: The results showed that intra-LPGi injection of 0.8 &#956;mol of 17&#946;-estradiol attenuated the chronic phase (P&#60;0.001) of paw jerking behaviour. CNQX significantly prevented the antinociceptive effect of intra-LPGi 17&#946;-estradiol both in the acute (P&#60;0.05) and in the chronic phase (P&#60;0.001) of formalin test. Conclusion: Considering the results of this study, it can be concluded that the analgesic effect of intra-LPGi injection of 17&#946;-estradiol might be mediated via AMPA receptors.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>147</FPAGE>
			<TPAGE>154</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/122017/01/232017/01/302016/11/132017/01/272016/10/292016/10/8
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/7/17
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/82017/05/192017/05/232017/01/112017/05/232017/03/172017/03/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/12/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Roghaieh</Name>
				<MidName></MidName>
				<Family>Khakpay</Family>
				<NameE>Roghaieh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khakpay</FamilyE>
				<Organizations>
				<Organization>Department of Animal Sciences, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>rkhakpai@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maryam</Name>
				<MidName></MidName>
				<Family>Azaddar</Family>
				<NameE>Maryam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Azaddar</FamilyE>
				<Organizations>
				<Organization>Department of Animal Sciences, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>maryam.azaddar@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>17β-Estradiol</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Paragigantocellularis lateralis nucleus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>AMPA receptors</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Formalin test.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Aloisi A, Ceccarelli I. Role of gonadal hormones in formalin-induced pain responses of male rats: modulation by estradiol and naloxone administration. Neuroscience. 1999;95(2):559-566.##Aloisi A, Ceccarelli I, Lupo C. Behavioural and hormonal effects of restraint stress and formalin test in male and female rats. Brain research bulletin. 1998;47,57-62.##Andrezik JA, Chan-Palay V, Palay SL. The nucleus paragigantocellularis lateralis in the rat. Anatomy and embryology. 1981;161(4):373-390.##Arita H, Kogo N, Ichikawa K. Locations of medullary neurons with non-phasic discharges excited by stimulation of central and/or peripheral chemoreceptors and by activation of nociceptors in cat. Brain research. 1988;442(1):1-10.##Aston-Jones G, Chiang C, Alexinsky T. Discharge of noradrenergic locus coeruleus neurons in behaving rats and monkeys suggests a role in vigilance. Progress in brain research. 1991;88:501-520.##Azhdari-Zarmehri H, Rahmani A, Puzesh S, Erami E, Emamjomeh M. Assessing the Effect of Lidocaine Injection into the Nucleus Paragigantocellularislateralis on Formalin Test and Hot Plate Test Induced Nociceptive Behaviors in Rats. ZUMS Journal. 2013a;21(85):10-29.##Azhdari-Zarmehri H, Reisi Z, Vaziri A, Haghparast A, Shaigani P, Haghparast A. Involvement of orexin-2 receptors in the ventral tegmental area and nucleus accumbens in the antinociception induced by the lateral hypothalamus stimulation in rats. Peptides. 2013b;47:94-98.##Craft RM, Mogil JS, Aloisi AM. Sex differences in pain and analgesia: the role of gonadal hormones. European Journal of Pain. 2004;8,397-411.##Dubuisson D and Dennis SG. The formalin test: a quantitative study of the analgesic effects of morphine, meperidine, and brain stem stimulation in rats and cats. Pain. 1978; 4,161-174.##Engelman HS, Allen TB, MacDermott AB. The distribution of neurons expressing calcium-permeable AMPA receptors in the superficial laminae of the spinal cord dorsal horn. The Journal of neuroscience. 1999; 19(6):2081-2089.##Erami E, Azhdari-Zarmehri H, Ghasemi-Dashkhasan E, Esmaeili M-H, Semnanian S. Intra-paragigantocellularis lateralis injection of orexin-A has an antinociceptive effect on hot plate and formalin tests in rat. Brain research. 2012;1478:16-23.##Fathi-Moghaddam H, Kesmati M, Mohammad Pour Kargar H. The effect of paragigantocellularis lateralis lesion on conditioned place preference (CPP) in presence or absence of a 2 adrenergic agonist (clonidine) in male rats. Acta Physiologica Hungarica. 2006;93(1):33-40.##Foy MR, Xu J, Xie X, Brinton RD, Thompson RF, Berger TW. 17β-estradiol enhances NMDA receptor-mediated EPSPs and long-term potentiation. Journal of Neurophysiology. 1999; 81(2):925-929.##Gangadharan V, Wang R, Ulzhöfer B, Luo C, Bardoni R, Bali KK, Agarwal N, Tegeder I, Hildebrandt U, Nagy GG, Todd AJ. Peripheral calcium-permeable AMPA receptors regulate chronic inflammatory pain in mice. The Journal of clinical investigation. 2011;121(4):1608-1623. ##Gebhart GF. Descending modulation of pain. Neuroscience &#38; Biobehavioral Reviews. 2004;27(8): 729-737.##Gordon FT, Soliman MR. The effects of estradiol and progesterone on pain sensitivity and brain opioid receptors in ovariectomized rats. Hormones and behavior. 1996;30(3):244-250.##Grassi S, Frondaroli A, Scarduzio M, Dutia MB, Dieni C, Pettorossi VE. Effects of 17β-estradiol on glutamate synaptic transmission and neuronal excitability in the rat medial vestibular nuclei. Neuroscience. 2010;165(4):1100-1114.##Grassi S, Frondaroli A, Scarduzio M, Dieni CV, Brecchia G, Boiti C, Pettorossi VE. Influence of sex and estrous cycle on synaptic responses of the medial vestibular nuclei in rats: role of circulating 17β-estradiol. Brain research bulletin. 2012;87(2):319-327.##Hajszan T, MacLusky NJ, Leranth, C. Role of androgens and the androgen receptor in remodeling of spine synapses in limbic brain areas. Hormones and behavior. 2008;53(5):638-646.##Hartmann B, Ahmadi S, Heppenstall PA, Lewin GR, Schott C, Borchardt T, Seeburg PH, Zeilhofer HU, Sprengel R, Kuner R. The AMPA receptor subunits GluR-A and GluR-B reciprocally modulate spinal synaptic plasticity and inflammatory pain. Neuron. 2004;44(4):637-650.##Hayashi T. Evolutionarily conserved palmitoylation-dependent regulation of ionotropic glutamate receptors in vertebrates. Neurotransmitter. 2014;1. ##Isgor C, Sengelaub DR. Effects of neonatal gonadal steroids on adult CA3 pyramidal neuron dendritic morphology and spatial memory in rats. Journal of neurobiology. 2003;55(2):179-190.##Khakpay R, Semnanian S, Javan M, Janahmadi M. The effect of intra-locus coeruleus injection of 17β-estradiol on inflammatory pain modulation in male rat. Behavioural brain research. 2010;214(2):409-416.##Khakpay R, Barani S, Hatami Nemati H. The antinociceptive effect of 17β-estradiol in the paragigantocellularis lateralis of male rats is mediated by estrogenic receptors. Physiology and Pharmacology. 2014;18(2):215-223.##Malinow R, Malenka RC. AMPA receptor trafficking and synaptic plasticity. Annual review of neuroscience. 2002;25(1):103-126.##Malmberg AB, Yaksh TL. Antinociceptive actions of spinal nonsteroidal anti-inflammatory agents on the formalin test in the rat. Journal of Pharmacology and Experimental Therapeutics. 1992; 263(1):136-146.##Paxinos G, Watson C. The rat brain in stereotaxic coordinates-The New Coronal Set: Academic press;  2005. ##Sakuma Y. Gonadal steroid action and brain sex differentiation in the rat. Journal of neuroendocrinology. 2009;21(4):410-414.##Tong CK, MacDermott AB. Both Ca2+‐permeable and‐impermeable AMPA receptors contribute to primary synaptic drive onto rat dorsal horn neurons. The Journal of physiology. 2006; 575(1):133-44##Van Bockstaele E, Akaoka H, Aston-Jones G. Brainstem afferents to the rostral (juxtafacial) nucleus paragigantocellularis: integration of exteroceptive and interoceptive sensory inputs in the ventral tegmentum. Brain research. 1993;603(1):1-18.##Wang Y, Wu J, Wu Z, Lin Q, Yue Y, Fang L. Regulation of AMPA receptors in spinal nociception. Molecular Pain. 2010;6(1):1.##Wheeler-Aceto H, Cowan A. Neurogenic and tissue-mediated components of formalin-induced edema: evidence for supraspinal regulation. Agents and actions. 1991;34(1-2):264-269.##Wong M, Moss RL. Long-term and short-term electrophysiological effects of estrogen on the synaptic properties of hippocampal CA1 neurons. The Journal of neuroscience. 1992; 12(8):3217-3225.##Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000; 288(5472):1765-1768.#### ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Effects of selenium nanoparticles on kidney and liver functional disorders in streptozotocin-induced diabetic rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Diabetes mellitus, as a chronic metabolic disease, is associated with a wide range of kidney and liver disorders. The goal of this study was to indicate the effects of selenium nanoparticles on the function of kidney and liver enzymes in stereptozocin induced diabetic rats. Methods: In this study, 35 male wistar rats were divided into five groups (n=7): control, diabetic control and three experimental groups receiving selenium nanoparticle solutions at doses of 0.1, 0.2 and 0.4 mg/kg/BW respectively. To induce diabetes in rats, a single dose of streptozocin (60 mg/kg/BW) was injected intraperitoneally. After the experimental period, blood samples were collected from all groups and the blood factors associated with the liver enzymes and kidney factors were measured and analyzed. Results: The results indicated that the levels of fasting blood sugar in all groups treated with selenium nanoparticles had a significant reduction compared to the diabetic group (P&#8804;0.05). Aspartate amino transferase had a significant reduction at the maximum dose compared to the diabetic group (P&#8804; 0.05). Also a significant decrease in the level of albumin was seen in the group treated with selenium nanoparticle (P&#8804; 0.05). Selenium nanoparticle treatment made a significant decreases in the levels of urea and ceratinine at the maximum dose (P&#8804; 0.05). Conclusion: The consumption of selenium nanoparticles in proper dosages may have beneficial effects on diabetic complications by lowering blood sugar as well as reducing the increased levels of the liver enzymes and kidney factors, albumin and cratinine resulting in the better function of kidney and liver.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>155</FPAGE>
			<TPAGE>162</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/122017/01/232017/01/302016/11/132017/01/272016/10/292016/10/82016/09/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/7/4
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/82017/05/192017/05/232017/01/112017/05/232017/03/172017/03/152017/01/22
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/11/3
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mahnaz</Name>
				<MidName></MidName>
				<Family>Rezaei-Kelishadi</Family>
				<NameE>Mahnaz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rezaei-Kelishadi</FamilyE>
				<Organizations>
				<Organization>Department of Biochemistry, Payame Noor University of Esfahan, Esfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>m.rezaie81@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ali</Name>
				<MidName></MidName>
				<Family>Ghasemi</Family>
				<NameE>Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ghasemi</FamilyE>
				<Organizations>
				<Organization>Department of Biochemistry, Payame Noor University of Esfahan, Esfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>alighasemi03@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Nasser</Name>
				<MidName></MidName>
				<Family>Nabi Abdolyosefi</Family>
				<NameE>Nasser</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Nabi Abdolyosefi</FamilyE>
				<Organizations>
				<Organization>Department of Biochemistry, Payame Noor University of Esfahan, Esfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>naser_nabi88@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Setareh</Name>
				<MidName></MidName>
				<Family>Zamani-Doabi</Family>
				<NameE>Setareh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Zamani-Doabi</FamilyE>
				<Organizations>
				<Organization>Department of Biochemistry, Payame Noor University of Esfahan, Esfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>sk_9678@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Majid</Name>
				<MidName></MidName>
				<Family>Ramezani</Family>
				<NameE>Majid</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ramezani</FamilyE>
				<Organizations>
				<Organization>Department of Internal Medicine, Baghiatallah University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Saeed</Name>
				<MidName></MidName>
				<Family>Changizi-Ashtiyani</Family>
				<NameE>Saeed</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Changizi-Ashtiyani</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>ashtiyani@sums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Azar</Name>
				<MidName></MidName>
				<Family>Rahimi</Family>
				<NameE>Azar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rahimi</FamilyE>
				<Organizations>
				<Organization>Department of Biochemistry, Payame Noor University of Esfahan, Esfahan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>ronak.r323@gmail.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Selenium</KeyText>
			</KEYWORD>

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

			<KEYWORD>
				<KeyText>Liver enzymes</KeyText>
			</KEYWORD>

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

		<REFRENCES>
			<REFRENCE>
				<REF>Ahmed HH, Abd El-Maksoud MD, Abdel Moneim AE, Aglan HA. Pre-Clinical Study for the Antidiabetic Potential of Selenium Nanoparticles. Biol Trace Elem Res.2016. [Epub ahead of print].##Al-Quraishy S, Dkhil MA, Moneim AEA. Anti-hyperglycemic activity of selenium nanoparticles in streptozotocin-induced diabetic rats. International journal of nanomedicine 2015;10:6741.##Anand P, Murali K, Tandon V, Chandra R, Murthy P. Preliminary studies on antihyperglycemic effect of aqueous extract of Brassica nigra (L.) Koch in streptozotocin induced diabetic rats. Indian journal of experimental biology  2007;45(8):696.##Dennert G1, Zwahlen M, Brinkman M, Vinceti M, Zeegers MP, Horneber M.. Selenium for preventing cancer. Cochrane Database Syst Rev 2011 May 11;(5):CD005195.##Di Naso FC, Simões Dias A, Porawski M, Marroni NA. Exogenous superoxide dismutase: action on liver oxidative stress in animals with streptozotocin-induced diabetes. Experimental diabetes research  2011;2011:754132.##Dkhil MA, Al-Quraishy S, Diab MM, Othman MS, Aref AM, Moneim AEA. The potential protective role of Physalis peruviana L. fruit in cadmium-induced hepatotoxicity and nephrotoxicity. Food and Chemical Toxicology  2014;74:98-106. ##Gandhi GR, Sasikumar P. Antidiabetic effect of Merremia emarginata Burm. F. in streptozotocin induced diabetic rats. Asian Pac J Trop Biomed. 2012;2(4):281-6. ##Gayathri M, Kannabiran K. Hypoglycemic activity of Hemidesmus indicus R. Br. on streptozotocin-induced diabetic rats. International journal of diabetes in developing countries 2008;28(1):6.##Giacco F, Brownlee M. Oxidative stress and diabetic complications. Circulation research  2010;107(9):1058-70.##Guney M, Erdemoglu E, Mungan T. Selenium–Vitamin E Combination and Melatonin Modulates Diabetes-Induced Blood Oxidative Damage and Fetal Outcomes in Pregnant Rats. Biological trace element research 2011;143(2):1091-102.##Harmon JS, Bogdani M, Parazzoli SD, Mak SS, Oseid EA, Berghmans M, et al. β-Cell-specific overexpression of glutathione peroxidase preserves intranuclear MafA and reverses diabetes in db/db mice. Endocrinology 2009;150(11):4855-62.##Hassanin KM, El-Kawi SHA, Hashem KS. The prospective protective effect of selenium nanoparticles against chromium-induced oxidative and cellular damage in rat thyroid. International journal of nanomedicine  2013;8:1713.##Hei Y-j, Farahbakhshian S, Chen X, Battell ML, McNeill JH. Stimulation of MAP kinase and S6 kinase by vanadium and selenium in rat adipocytes. Molecular and cellular biochemistry 1998;178(1-2):367-75.##Imai H. Biological significance of lipid hydroperoxide and its reducing enzyme, phospholipid hydroperoxide glutathione peroxidase, in mammalian cells. Yakugaku Zasshi  2004 Dec;124(12):937-57.##Jablonska E, Reszka E, Gromadzinska J, Wieczorek E, Krol MB, Raimondi S, et al. The Effect of Selenium Supplementation on Glucose Homeostasis and the Expression of Genes Related to Glucose Metabolism. Nutrients. 2016;8(12). pii: E772.##Jia X, Liu Q, Zou S, Xu X, Zhang L. Construction of selenium nanoparticles/β-glucan composites for enhancement of the antitumor activity. Carbohydrate polymers 2015;117:434-42.##Kajbaf F, Mojtahedzadeh M, Abdollahi M. Mechanisms underlying stress-induced hyperglycemia in critically ill patients. Therapy 2007; 4: 97-106.##Kilinc M, Guven MA, Ezer M, Ertas IE, Coskun A. Evaluation of serum selenium levels in Turkish women with gestational diabetes mellitus, glucose intolerants, and normal controls. Biological trace element research 2008;123(1-3):35-40.##Kim HK, Kim MJ, Lyu ES, Shin D-H. Improvement of diabetic complication by hydrangea dulcis folium in streptozotocin-induced diabetic rats. Biological and Pharmaceutical Bulletin 2009;32(1):153-6.##Kim S-S, Koo J-H, Kwon I-S, Oh Y-S, Lee S-J, Kim EJ, et al. Exercise training and selenium or a combined treatment ameliorates aberrant expression of glucose and lactate metabolic proteins in skeletal muscle in a rodent model of diabetes. Nutrition research and practice 2011;5(3):205-13.##Kornhauser C, Garcia-Ramirez JR, Wrobel K, Pérez-Luque E-L, Garay-Sevilla M-E, Wrobel K. Serum selenium and glutathione peroxidase concentrations in type 2 diabetes mellitus patients. Primary Care Diabetes 2008;2(2):81-5.##Kumar S, Singh R, Vasudeva N, Sharma S. Acute and chronic animal models for the evaluation of anti-diabetic agents. Cardiovascular diabetology 2012;11(1):1.##Laclaustra M, Navas-Acien A, Stranges S, Ordovas JM, Guallar E. Serum selenium concentrations and diabetes in US adults: National Health and Nutrition Examination Survey (NHANES) 2003-2004. Environmental health perspectives  2009;117(9):1409.##Lenzen S. The mechanisms of alloxan-and streptozotocin-induced diabetes. Diabetologia 2008;51(2):216-26.##Maiti S, Ali KM, Jana K, Chatterjee K, De D, Ghosh D. Ameliorating effect of mother tincture of Syzygium jambolanum on carbohydrate and lipid metabolic disorders in streptozotocin-induced diabetic rat: Homeopathic remedy. Journal of natural science, biology, and medicine 2013;4(1):68.##Messarah M, Klibet F, Boumendjel A, Abdennour C, Bouzerna N, Boulakoud MS, et al. Hepatoprotective role and antioxidant capacity of selenium on arsenic-induced liver injury in rats. Experimental and toxicologic pathology 2012;64(3):167-74.##Miyamoto Y, Koh YH, Park YS, Fujiwara N, Sakiyama H, Misonou Y, et al. Oxidative stress caused by inactivation of glutathione peroxidase and adaptive responses. Biological chemistry 2003;384(4):567-74.##Nabi SA, Kasetti RB, Sirasanagandla S, Tilak TK, Kumar MVJ, Rao CA. Antidiabetic and antihyperlipidemic activity of Piper longum root aqueous extract in STZ induced diabetic rats. BMC complementary and alternative medicine 2013;13(1):1.##Oztürk Z, Gurpinar T, Vural K, Boyacıoglu S, Korkmaz M, Var A. Effects of selenium on endothelial dysfunction and metabolic profile in low dose streptozotocin induced diabetic rats fed a high fat diet. Biotechnic &#38; Histochemistry 2015;90(7):506-15.##Park K, Rimm EB, Siscovick DS, Spiegelman D, Manson JE, Morris JS, et al. Toenail selenium and incidence of type 2 diabetes in US men and women. Diabetes Care 2012;35(7):1544-51.##Raddatz D, Ramadori G.Carbohydrate metabolism and the liver: actual aspects from physiology and disease. Z Gastroenterol 2007;45(1):51-62.##Rezaei M, Zamani S, Ghasemi A, Rahimi A, Nabi N, Changizi- Ashtiyani S, Ramezani M, Zarei A. The Effects of Hydroalcoholic Extract of Melissa officinalis .L on the Level of Renal Function and Liver Enzymes in Diabetic Rats. Iranian Journal of Endocrinology and Metabolism. 2016; 17 (5): 353-361. ##Shaw JE, Sicree RA, Zimmet PZ. Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes research and clinical practice 2010;87(1):4-14.##Son DJ, Hwang SY, Kim M-H, Park UK, Kim BS. Anti-Diabetic and Hepato-Renal Protective Effects of Ziyuglycoside II Methyl Ester in Type 2 Diabetic Mice. Nutrients 2015;7(7):5469-83.##Srivastava P, Braganca JM, Kowshik M. In vivo synthesis of selenium nanoparticles by Halococcus salifodinae BK18 and their anti‐proliferative properties against HeLa cell line. Biotechnology progress 2014;30(6):1480-7.##Stapleton SR. Selenium: an insulin mimetic. Cellular and Molecular Life Sciences CMLS 2000;57(13-14):1874-9.##Steinbrenner H, Sies H. Protection against reactive oxygen species by selenoproteins. Biochimica et Biophysica Acta (BBA)-General Subjects 2009;1790(11):1478-85.##Thiruvenkatasubramaniam R, Jayakar B. Anti-hyperglycemic and anti-hyperlipidaemic activities of Bauhinia variegata L on streptozotocin induced diabetic rats. Der Pharmacia Lettre 2010;2(5):330-4.##Torres S, Campos V, León C, Rodríguez-Llamazares S, Rojas S, Gonzalez M, et al. Biosynthesis of selenium nanoparticles by Pantoea agglomerans and their antioxidant activity. Journal of nanoparticle research 2012;14(11):1-9.##Wang H, Zhang J, Yu H. Elemental selenium at nano size possesses lower toxicity without compromising the fundamental effect on selenoenzymes: comparison with selenomethionine in mice. Free Radical Biology and Medicine 2007;42(10):1524-33.##Zeng J, Zhou J, Huang K. Effect of selenium on pancreatic proinflammatory cytokines in streptozotocin-induced diabetic mice. The Journal of nutritional biochemistry 2009;20(7):530-6.##Zhang J, Wang H, Yan X, Zhang L. Comparison of short-term toxicity between Nano-Se and selenite in mice. Life sciences 2005;76(10):1099-109.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Swertia longifolia Boiss has beneficial effects on hepatic and renal functions in diabetic rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Diabetes is a multifactorial syndrome with high prevalence which may induce serious disorders in the body organs like the liver and kidney. This study aimed to compare the effects of the alcoholic extract of the aerial parts of Swertia longifolia Boiss on blood glucose, lipid profiles and liver and kidney function tests in streptozotocin-induced diabetes. Methods: Thirty five male rats were put into five groups: control, diabetic control and three diabetic experimental groups which were gavaged with alcoholic extract of Swertia longifolia Boiss at doses of 100 and 200 mg/kg BW and glibenclamide at a dose of 10 mg/kg BW, respectively. Diabetes was induced by intraperitoneal injection of streptozotocin. At the end of day 21 blood samples were collected from all groups and the blood factors were measured and analyzed. Results: The levels of creatinine, urea, liver enzymes, cholesterol and low density lipoprotein increased in the diabetic control group compared to the control, while the mentioned factors in the groups receiving Swertia longifolia Boiss alcoholic extract decreased significantly (P&#60;0.05). In the experimental group receiving glibenclamide, the levels of creatinine, urea and lipid profiles also decreased, while the levels of liver enzymes and insulin significantly increased (P&#60;0.05). Conclusion: The consumption of the alcoholic extract of the aerial parts of Swertia longifolia Boiss by lowering lipid profiles, liver enzymes, creatinine and urea as well as increasing insulin levels had beneficial effects on the hepatic and renal functions and could alleviate the symptoms of increased glucose and hyperlipidemia in diabetic rats.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>163</FPAGE>
			<TPAGE>171</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/12/122017/01/232017/01/302016/11/132017/01/272016/10/292016/10/82016/09/252016/10/2
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/7/11
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2017/03/82017/05/192017/05/232017/01/112017/05/232017/03/172017/03/152017/01/222017/01/11
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/10/22
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Ali</Name>
				<MidName></MidName>
				<Family>Zarei</Family>
				<NameE>Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Zarei</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, School of Nursing Hazrat Zahra (P.B.U.H) Abadeh, Shiraz University of Medical Sciences, Shiraz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>zarei.ali40@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ali Akbar</Name>
				<MidName></MidName>
				<Family>Malekirad</Family>
				<NameE>Ali Akbar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Malekirad</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Payame Noor University,Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>ak_malekirad@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad</Name>
				<MidName></MidName>
				<Family>Abdollahi</Family>
				<NameE>Mohammad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Abdollahi</FamilyE>
				<Organizations>
				<Organization>Faculty of Pharmacy, Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>Mohammad.Abdollahi@UToronto.Ca</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Gholamhassan</Name>
				<MidName></MidName>
				<Family>Vaezi</Family>
				<NameE>Gholamhassan</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Vaezi</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>gh.vaezi@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Saeed</Name>
				<MidName></MidName>
				<Family>Changizi-Ashtiyani</Family>
				<NameE>Saeed</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Changizi-Ashtiyani</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Arak University of Medical Sciences, Arak, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>ashtiyani@sums.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


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

			<KEYWORD>
				<KeyText>Liver</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Kidney</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Streptozotocin</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Swertia longifolia Boiss</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
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Effect of insulin on the metabolism of adipose tissue from normal rats. J Biol Chem1952.;194:33-40.##Hui H, Dotta F, Di Mario U, Perfetti R.. Role of caspases in the regulation of apoptotic pancreatic islet beta-cells death. J Cell Physiol 2004;200:177-200.##Jamwal A. Systematic.. Review on Xanthones and Others Isolates From Genus Swertia. International Journal of Pharmaceutical and Chemical Sciences 2012;1 .1468-1482.##Jaya Preethi Peesa.. Herbal Medicine for Diabetes Mellitus: A Review. International Journal of Phytopharmacy 2013; 1:1-22.##Kameswararao B, Kesavulu MM, APParao C. Evaluation of Antidiabetic Effect of Momordica Cymbalaria Fruit in Alloxandiabetic Rats. FitoteraPia 2003;74:7-13.##Kawanishi, K, Ueda, H, and Moriyasu M.. Aldose Reductase Inhibitors from the Nature. Curr. Med. Chem 2003;10, 1353-1374.##Lenzen S. The mechanisms of alloxan- and streptozotocin-induced diabetes. Diabetologia 2008;51:216-26. ##Lin Y, Sun Z. Current Views on Type 2 Diabetes. 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			</REFRENCE>
		</REFRENCES>

	</ARTICLE>

</ARTICLES>

</JOURNAL>
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