摘要
Gallic acid (GA) comes under the category of polyphenolic compounds and has antioxidant properties. Gallic acid has been ameliorating the cardiac ischemia-reperfusion injury in rodents. Still the activity of GA remains unknown in diabetic rats, So the current study is performed to explore the possible mechanisms of GA in a diabetic rodent model of ischemia-reperfusion (I/R) injury induced by streptozotocin (STZ). Single injection of STZ was used for induction the diabetes and the Wistar rats categorized into 5 groups and 8 number of rats in each group. IR injury were carried out in the rats via ischemia (45 min following reperfusion (60 min). Body weight, organ weight, glucose, insulin level was scrutinized. Antioxidant, renal, lipid, cardiac parameters and inflammatory cytokines were also analyzed.GA treatment significantly (p <0.001) suppressed the glucose level, glycated hemoglobin level and improved the insulin level. GA treatment also enhanced the body weight and suppressed the renal weight. GA treatment significantly (p < 0.001) reduced the level of malonaldehyde (MDA) and enhanced the level of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and 8-oxo-7,8-dihydro-2' -deoxyguanosine (8-OHdG). GA treatment significantly (p < 0.001) reduced the level of lactate dehydrogenase (LDH) and creatine kinase myocardial band (CK-MB). GA treatment significantly (p < 0.001) altered the level of lipid parameters and suppressed the level of inflammatory cytokines. Taken together, this study reveals the therapeutic effect of gallic acid and protects the diabetic heart from ischemia-reperfusion injury via activation of the potassium channel.
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