Oxidative stress is a biological entity quoted as accountable for several pathological conditions including diabetes mellitus. Chronic hyperglycemia in diabetes is associated with oxidative stress mediated tissue damage. The present study is aimed to explore the role of fisetin, in ameliorating hyperglycemia-mediated oxidative damage to liver in streptozotocin induced diabetic rats. In addition to the levels of blood glucose, plasma insulin, glycosylated hemoglobin, the extent of oxidative stress was assessed by hepatic lipid peroxides and hydroperoxides. The levels of reduced glutathione and the activities of enzymatic antioxidants were determined in the liver tissues. The activities of serum aminotransferases and alkaline phosphatase were assayed. A portion of liver was processed for histological and ultrastructural studies. Oral administration of fisetin (10 mg/kg b. w.) to diabetic rats decreased the levels of blood glucose and glycosylated hemoglobin and increased the plasma insulin level. A reduction in lipid peroxides and hydroperoxides were observed. The diminished activities of antioxidant enzymes and reduced glutathione in diabetic rats were improved upon fisetin administration. Thus, the results of the present study indicate that fisetin treatment protects the hepatocytes by improving the antioxidant competence in hepatic tissues of diabetic rats which is further evidenced from histological and ultra structural observations.
Keywords: Antioxidant; CAT; DMSO; Fisetin; GPx; GR; GSH; GST; HbAlc; Hepatocytes; Hyperglycemia; LSD; Oxidative stress; ROS; SD; SOD; STZ; TBARS; Tissue protective nature; catalase; dimethyl sulphoxide; glutathione S transferase; glutathione peroxidase; glutathione reductase; glycosylated hemoglobin; least significant difference; reactive oxygen species; reduced glutathione; standard deviation; streptozotocin; superoxide dismutase; thiobarbituric acid reactive substances.
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