Glimepiride reduces on experimentally induced ischemia/reperfusion in diabetic rats.

Hyperglycaemia is most probably a contributing factor in the development of ischaemic acute renal failure (ARF) in many patients. Both clinical and experimental data suggest that hyperglycaemia increases the risk of ARF. Present study was designed to evaluate in Glimepiride reduced on experimentally induced ischemia/reperfusion in diabetic rats. Type 2 Diabetes was induced in rats by a single intraperitoneal (i.p) injection of Streptozotocin (65 mg/kg, STZ) in overnight fasting rats followed by the i.p administration of Nicotinamide (110 mg/kg, NIC) after 15 minutes. After right nephrectomy, Glimepiride (0.5 mg/kg/day, p.o) was administered for 15 days. On the 16th day, ischemia was induced in contra lateral kidney for 45 min, followed by reperfusion for 24 hr. Renal function marker and oxidative parameter were estimated at the end of 24 hr reperfusion. At the end of experimental period the level of malondialdehyde formation/ lipid peroxidation (LPO) in kidney tissue and serum marker Creatinine, Urea and Uric acids were significantly increased. Whereas, the activity of biomarkers of oxidative stress such as reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) were found to be decreased significantly compared to control rats. Glimepiride improved the Serum Uric acid and tissues parameter LPO after renal ischemia/reperfusion injury in diabetic rats. In conclusion, Glimepiride shows low may improve experimentally induced ischemia/reperfusion in type 2 diabetic rats.