Oxidative stress response in diabetic nephropathy rats following injection of embryonic stem cells via the tail vein / 中国组织工程研究

ABSTRACT

BACKGROUND:Occurrence and development of diabetic complications is closely related to the severity of oxidative stress imbalance in the body. OBJECTIVE:To investigate the effect of embryonic stem cel s on oxidative stress response of rats with diabetic nephropathy. METHODS:Primarily cultured rat embryonic stem cel s were observed for cel morphology and surface antigen detection. Sprague-Dawley rats were divided into experimental group (two injections of embryonic stem cel s via the tail vein), model group (injection of the same volume of PBS), and normal control group (with no modeling, intraperitoneal injection of sodium citrate-citrate buffer). In the former two groups, the rats were intraperitoneal y injected sodium citrate-citrate buffer diluted streptozotocin to establish diabetic nephropathy models before treatment. At 5 weeks after the last injection, blood glucose level, renal function indicators (urine protein/urine creatinine, blood urea nitrogen and serum creatinine) were tested in each group;contents of malondialdehyde and protein carbonyl were detected in the kidney;the expression level of superoxide dismutase was detected by western blot assay. RESULTS AND CONCLUSION:The embryonic stem cel s were oval or round, with clear boundary and good refraction, and highly expressed Oct-4 and SSEA-1. Compared with the control group, renal biochemical indicators, malondialdehyde and protein carbonyl contents were significantly increased, while the expression level of superoxide dismutase was decreased dramatical y in the model group and experimental group (P<0.05);compared with the model group, the renal biochemical indicators, malondialdehyde and protein carbonyl contents were dropped significantly in the experimental group, but the expression of superoxide dismutase was significantly rebounded (P<0.05). Taken together, embryonic stem cel s can reverse the occurrence and development of diabetic nephropathy by inhibiting oxidative stress in progress.