Abstract: ABSTRACT: Objective To investigate the effect and mechanism of pyrrolidine dithiocarbamate (PDTC) on islet β cell oxidative injury in type 2 diabetic rats. Methods Type 2 diabetic rats model were set up by long-term feeding high-fat foods accompanied with a single intraperitoneal injection of low dose of streptozotocin (STZ, 27mg/kg body weight). The rats in PDTC group were administerd with PDTC (50mg/kg/d) by intraperitoneal injection. After treatment for 1 week, blood glucose levels were estimated. Malondialdehyde (MDA), Superoxide dismutase (SOD) and Glutathione peroxidase (GSH-PX) content in pancreatic tissue were measured. The expression of inducible nitric oxide synthase (iNOS) and the prouduction of nitrotyrosine (NT) in islet tissue were examined by using immunohistochemistry and Western blot. The rate of pancreatic islet β cell apoptosis was detected by flow cytometry. Results The blood glucose level, MDA content, pancreatic β-cell apoptosis, iNOS expression and NT production were significantly higher, while the SOD and GSH-PX activities were significantly lower in DM group than those in normal control group (P<0.01). After administration of PDTC, The level of blood glucose, MDA content, pancreatic β-cell apoptosis, iNOS expression and NT production were significantly decreased, while the SOD and GSH-PX activities were markedly increased when compared with DM group (P＜0.01). Conclusion PDTC can reduce the level of blood glucose, relieve the oxidative stress reaction of diabetic rats, suppress the expression of iNOS and NT production, and decrease pancreatic islet β cell apoptosis in diabetic rats.

Key words: Pyrrolidine dithiocarbamate, Diabetes, oxidative injury, Pancreatic islet β cell, Apoptosis