Resveratrol Reduces Focal Cerebral Ischemia-Reperfusion Injury in Diabetic Rats

• Main Authors: Yang Tzu Wu, 吳仰慈
• Other Authors: L. M. Hung
• Format: Others
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/89848517397562295890

碩士 === 長庚大學 === 生物醫學研究所 === 99 === Resveratrol(trans-3,4′,5-trihydroxystilbene), a natural antioxidant derived from grapes and also commonly found in red wine, has exerted antihyperglycemic effects in streptozotocin(STZ)-induced type I diabetes as well as improve insulin sensitivity in diet-induced insulin resistant animal models. Additionally, our prior studies showed that resveratrol suppressed infarct volume and exerted neuroprotective effects on rats subjected to focal cerebral ischemia(FCI) injury. However, it remains unknown whether resveratrol can protect against FCI injury in STZ-induced hyperglycemic rats, and its underlying mechanisms. In the present study, Long Evans rats were used and grouped into age-matched non-diabetic controls, STZ-induced diabetics, and resveratrol treated (1, 10, or 100 μg/kg/day for one week) diabetics. Rats were subjected to 1 hour of middle cerebral artery(MCA) occlusion followed by 24 hours of reperfusion. Results show that FCI-induced infarct volumes increased significantly in STZ-diabetic rats as compared with non-diabetic controls, suggesting that diabetic hyperglycemia may aggravate ischemia-reperfusion(I/R)- injury. In the resveratrol treated diabetic rats, the infarct volumes were reduced significantly when compared with STZ-diabetic rats, but inflammatory cytokines (IL-1β, IL-6, and TNF-α) were not significantly different among the groups. Moreover, resveratrol treated diabetic rats exhibited improvement in neurological performances when compared to non-treated diabetic controls, and up-regulated protein expressions of estrogen receptor. Our results indicate that resveratrol might be a potent neuroprotective agent in diabetic individuals with ischemic stroke, and the underlying mechanism might be through altering the expressions of estrogen receptor.