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dc.contributor.authorSoufi, FG
dc.contributor.authorVardyani, M
dc.contributor.authorSheervalilou, R
dc.contributor.authorMohammadi, M
dc.contributor.authorSomi, MH
dc.date.accessioned2018-08-26T08:04:14Z
dc.date.available2018-08-26T08:04:14Z
dc.date.issued2012
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/49505
dc.description.abstractThis study was designed to investigate the possible effectiveness of chronic resveratrol administration on redox state, inflammatory mediators and apoptosis rate in diabetic rats. Male Wistar rats were divided into four groups (n = 6): normal control, diabetic control, normal rats treated with resveratrol, and diabetic rats treated with resveratrol. Diabetes was induced by injection of streptozotocin (50 mg/kg; i.p.), 15 min after the prescription of nicotinamide (110 mg/kg; i.p.) in 12 h-fasted rats. Four-month oral resveratrol administration (5 mg/kg/day) significantly alleviated hyperglycemia, weight loss, enhancement of oxidative markers (lipid peroxidation index, nitrite/nitrate content and oxidized to reduced glutathione ratio) and superoxide dismutase activity in diabetic rats. Moreover, resveratrol administration to diabetic rats improved the elevated levels of plasma TNF alpha and IL-6 as well as NF-kappa B activity of polymorphonuclear cells. On the other hand, four months resveratrol administration decreased the apoptosis rate in the kidney, heart, retina, sciatic nerve and the polymorphonuclear cells of diabetic rats. These beneficial antidiabetic observations suggest that treatment with resveratrol may be considered as a therapeutic approach to reduce diabetic-related complications.
dc.language.isoEnglish
dc.relation.ispartofGENERAL PHYSIOLOGY AND BIOPHYSICS
dc.subjectDiabetes
dc.subjectAntioxidant
dc.subjectHyperglycemia
dc.subjectRedox state
dc.subjectCell death
dc.titleLong-term treatment with resveratrol attenuates oxidative stress pro-inflammatory mediators and apoptosis in streptozotocin-nicotinamide-induced diabetic rats
dc.typeArticle
dc.citation.volume31
dc.citation.issue4
dc.citation.spage431
dc.citation.epage438
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.4149/gpb_2012_039


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