Protective Effect Of Vitamin C On Primary C57 Mice Renal Tubular Epithelial Cell Injury Induced By Oxidative Stress

Objective:Increased oxidative stress have been implicated in a variety of kidney diseases,such as renal ischemia-reperfusion(I/R)injury caused by shock or during surgery or transplantation,diabetic nephropathy and chronic tubulointerstitial injury.It is mediated by reactive oxygen species(ROS),including free radicals such as superoxide ions and hydroxyl radicals as well as non-free radical species such as hydrogen peroxide(H2O2).In order to study the reaction mechanism,using the hydrogen peroxide-induced C57 murine primary renal tubular epithelial cells structure of oxidative damage in vitro model.To know the protective effect of a certain concentration of vitamin C on damage and apoptosis in renal tubular epithelial cells from oxidative primary C57 mice.Method:In vitro cultured primary renal tubular epithelial cells in C57 mice are divided into four groups for the control group,hydrogen peroxide injury group,the vitamin C group,select 500?mol/L as a model to give different concentractions of vitamin C protection group.All groups are determined by MTT cell viability.SOD,MDA and total protein content are meadured 12h after cell stimulation to observe the cellular injury situation.Results:Compared with the control group,concentration of H2O2 in 150?mol/L or more would cause significant oxidative damage to the primary C57 mice renal tubular epithelial cells.Firstly,the cell viability and cell morphology were reduced and deformed significantly.secondly,the SOD activity and total protein content of cells were decreased but the MDA levels increased within certain range.Therefore,certain concentration of vitamin C can effectively resist oxidative damage induced by H2O2.Conclusion:1.a certain concentration of H2O2 in 150?mol/L can induce the primary C57 mice renal tubular epithelial cells oxidative damage and affect the cell viability.2.Vitamin C at 50?mol/L can be effectivelly suppressed the decreased of cells activity and the phenomenon of oxidative damage caused by H2O2.