Evaluation of Ginkgo biloba in Diabetic Nephrotoxicity
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Nephrotoxicity is the major cause of morbidity and mortality in diabetes and it is the leading cause of end stage renal disease. Hyperglycemia induced oxygen free radicals cause oxidative stress and subsequent oxidative damages, leading cell and tissue injury. Sprague-Dawley rats of both sexes were divided into 4 groups, Control, Diabetic control , Diabetic + Ginkgo biloba and Diabetic + Vit E group . Blood urea, serum creatinine and serum uric acid as well as plasma malondialdehyde, superoxide dismutase, catalase, reduced glutathione were estimated and histopathological studies of kidneys were performed. Alloxan at the dose of 120mg/kg i.p, for 2 months at the interval of 14 days, induced diabetes. This prolonged diabetes increased oxidative stress and caused an increase in the levels of serum creatinine, urea, uric acid and plasma malondialdehyde while there were decrease in the levels of superoxide dismutase, catalase and reduced glutathione in diabetic group as compared to normal control group. Histopathological examination revealed hemorrhage, necrosis, and infiltration of leukocytes around the glomerulus and interstitial spaces. Co-administration of Ginkgo biloba 300mg/kg orally, daily for 2 months in diabetic-induced rats caused decreased in the levels of serum creatinine, urea, uric acid and plasma malondialdehyde. Increased levels of superoxide dismutase, catalase and reduced glutathione were also found. The study revealed protective antioxidant activity of Ginkgo biloba in diabetic nephrotoxicity.
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