Beneficial Effect of Trimetazidine on Streptozotocin Induced Diabetic Nephropathy in Rats by Enhancing Glutathione Status.

Trimetazidine increase glutathione peroxidase and limits membrane damage caused by reactive oxygen species (ROS). It also has cytoprotective effect and limits the production of trimethylamine N-Oxide (TMAO) and provides the renoprotective effect. This study was designed to evaluate the renoprotective effect of trimetazidine (TMZ) in an experimental model of streptozotocin (STZ induced diabetic nephropathy in rats. For this experimental study sixty-six rats (66) were divided into eight groups. Group I (C1) and group II (C2) were normal healthy rat groups and sacrificed on 22nd day. Three groups of rats were induced diabetic nephropathy by streptozotocin (STZ) single intraperitonial administration at a dose of 50mg/kg body weight. Biochemical indices like serum blood sugar and the status of oxidative stress was assessed by renal cortical glutathione (GSH) levels. In streptozotocin treated groups, renal glutathione was significantly (p<0.01) lower when compared to control. In TMZ treated group, whereas renal glutathione was significantly (p<0.01) higher when compared with STZ induced nephropathy groups of rats. It may be assumed from this study that trimetazidine has nephroprotective effects because of its special antioxidant effects, which can delay the onset, severity and progression of nephropathy induced by streptozotocin in rats. Therefore, trimetazidine may be extensively studied in human with diabetic nephropathy for confirmation of its nephro-protective effects.