Abstract
ABSTRACTObjective: We designed this study to observe the effect of galangin on damaged mitochondria in the liver of diabetic rats.Methods: Male albino Wistar rats were made diabetic by injecting streptozotocin (STZ) intraperitoneally (40 mg kg−1 body weight (BW)). Galangin (8 mg kg−1 BW) or glibenclamide (600 µg kg−1 BW) was given orally daily once for 45 days to both healthy and diabetic rats.Results: Diabetic rats showed significant (P < 0.05) increase in liver mitochondrial oxidant [Thiobarbituric acid reactive substance (TBARS)] level and a significant decrease in enzymatic [superoxide dismutase (SOD), glutathione peroxidase (GPx)] and non-enzymatic (reduced glutathione (GSH)) antioxidant levels when compared with healthy rats. The mitochondrial enzymes isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (α-KGDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) and mitochondrial respiratory chain enzymes NADH-dehydrogenase and Cytochrome c-oxidase were decreased significantly (P < 0.05) in diabetic rats when compared with healthy rats. A natural flavonoid galangin administered to hyperglycemia-induced rats resulted in the following findings as compared to hyperglycemia-induced control rats: the oxidant levels decreased significantly (P < 0.05); the enzymatic and non-enzymatic antioxidant levels increased significantly (P < 0.05) and the function of mitochondrial enzymes and the mitochondrial respiratory chain enzymes increased significantly (P < 0.05).Conclusion: From the results, we conclude that galangin could maintain liver mitochondrial function in diabetic rats.
Highlights
Enhanced oxidative stress and decreased antioxidant status in diabetic patients and experimental animals contribute to the development of diabetic complications [1]
Prolonged hyperglycemia, increased production of free radicals, decreased antioxidant status, auto-oxidation of glycated proteins and increased lipid peroxidation play a major role in cellular apoptosis or necrosis in prolonged diabetic patients [2,3]
Once STZ was injected, 20% glucose was given for 24 h with drinking water for Figures 2 and 3 show the Thiobarbituric acid reactive substance (TBARS) concentration and enzymic (SOD, glutathione peroxidase (GPx)) and other (GSH) antioxidants in hepatic mitochondria of healthy and STZ-induced hyperglycemic rats
Summary
Enhanced oxidative stress and decreased antioxidant status in diabetic patients and experimental animals contribute to the development of diabetic complications [1]. Prolonged hyperglycemia, increased production of free radicals, decreased antioxidant status, auto-oxidation of glycated proteins and increased lipid peroxidation play a major role in cellular apoptosis or necrosis in prolonged diabetic patients [2,3]. The increased nitric oxide production, enhanced oxygen free radicals formation (OFRs) and enhanced protein glycation were caused by pancreatic β-cell damage in STZ-induced rats [4,5]. Enhanced free radical production in mitochondria may damage β-cells, leading to chronic diabetic complications [8]. We reported that the galangin reduces oxidative stress and enhances antioxidant in STZ-induced hyperglycemia [26]. We have designed this study to observe the galangin effect on oxidative mitochondrial damage in normal and STZ-induced hyperglycemic rats. In our study galangin was matched with glibenclamide in terms of its effectiveness as a standard antidiabetic agent
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