Effects of Resveratrol on Receptor for Advanced Glycation End Products (RAGE) Expression and Oxidative Stress in the Liver of Rats with Type 2 Diabetes. (14th October 2015)

• Record Type: Journal Article
• Authors: Khazaei, Mohammad; Karimi, Jamshid; Sheikh, Nasrin; Goodarzi, Mohammad Taghi; Saidijam, Massoud; Khodadadi, Iraj; Moridi, Heresh
• Is Part Of: Phytotherapy research. Volume 30:Number 1(2016)
• Page Start: 66
• Page End: 71
• Publication Date: 2015-10-14
• Subjects: resveratrol -- liver -- diabetes -- RAGE -- oxidative stress; Materia medica, Vegetable -- Periodicals; Botany, Medical -- Periodicals; Medicinal plants -- Periodicals; Plant Extracts -- therapeutic use -- Periodicals; Plants, Medicinal -- Periodicals; 581.634
• DOI: 10.1002/ptr.5501
• Languages: English
• ISSNs: 0951-418X

Abstract

Abstract : Incidence of diabetes mellitus is dramatically growing in the world. Oxidative stress, advanced glycation end products (AGEs) and receptor for AGE (RAGE) play key role in the pathogenesis of diabetes. Little is known about resveratrol effects on the liver. We hypothesize that resveratrol may exert a hepatoprotective effect in diabetic rats. Male rats with diabetes were treated with or without resveratrol at 1, 5 and 10 mg/kg body weight for 30 days. Total AGEs and malondialdehyde (MDA) levels in liver tissues were determined by spectrofluorimetric methods. Total antioxidant capacity and total oxidant contents in the liver and glucose in plasma were measured by a colorimetric assay. Expression of RAGE was assayed in liver of all animals using quantitative polymerase chain reaction. In liver tissue extract of resveratrol‐treated rats with diabetes, MDA levels, total oxidant, plasma glucose and expression of RAGE were significantly reduced compared to the untreated group. Moreover, total antioxidant levels were significantly increased in treated rats. There was no significant difference in AGE contents among all groups. These results revealed that resveratrol had beneficial effects on the liver by extenuating oxidative stress and down regulation of RAGE expression. Copyright © 2015 John Wiley & Sons, Ltd.