Seena, et al.: A Critical Study on Hypoglycaemic Effect of GlibenclamideThe present study is aimed to evaluate the hypoglycaemic effect of glibenclamide monotherapy on streptozotocin-induced diabetic rats and therapeutic impact of this agent on various organs by measuring the oxidative stress biomarker, lipid peroxidation and creatinine after a specific period of oral treatment. Eighteen male Wistar rats were taken of which twelve were randomly selected and diabetes was induced using streptozotocin (40 mg/kg) intraperitoneally, while 6 rats were vehicle injected. After inducing diabetes, the animals were grouped into healthy normal, diabetic control and diabetic test groups. The diabetic test rats were treated with glibenclamide (10 mg/kg) orally for 10 days continuously. On the 30th day of the experiment, all the animals were sacrificed and their blood and a portion of both the liver and pancreas were taken for biochemical analysis. The experimental parameters such as body weight, fasting blood glucose level, serum creatinine level and tissue lipid peroxidation status using malondialdehyde assay were investigated. All the results of the experimental data were analysed statistically using one-way analysis of variance using the SPSS 16. The current study reveals that glibenclamide treatment has a significant role in lowering the blood glucose but at the same time it increased the oxidative stress, which was reflected in the elevated malondialdehyde activity of both the hepatic and pancreatic tissues.

Objective:The objective of this study is to compare the antioxidant enzyme superoxide dismutase (SOD) level and lipid peroxidation product malondialdehyde (MDA) in ethanol treated non diabetic and diabetic rats. Methods: A total of 24 male Wistar albino rats were grouped as control (n=6), diabetic control (n=6), ethanol treated control (n=6) and ethanol treated test (n=6) groups. Total duration of this experiment was 30 days. Diabetes mellitus was induced in rats by a single intraperitoneal dose of streptozotocin at 40 mg/kg dissolved in 0.1 M cold citrate buffer. After the confirmation of diabetes