Atorvastatin preconditioning protect renal function against ischemia-reperfusion injury by increasing expression of endothelial nitric oxide synthase

Objective To investigate the protective effect of atorvastatin (ATO) preconditioning on rats with acute renal ischemia-reperfusion (I/R) injury and its effect on endothelial nitric oxide synthase (eNOS).Methods 18 male Sprague Dawley rat was randomly distributed into three groups:sham,I/R and I/R + ATO.ATO was given by intraperitoneal injection [20 mg/(kg·d)] 2 weeks before ischemia/ reperfusion operation in the I/R + ATO group.The sham group and I/R group received saline vehicle via the intraperitoneal route.Serum levels of blood urea nitrogen (BUN),creatinine (Cr),nitric oxide (NO) and expression levels of myeloperoxidase (MPO),eNOS and superoxide dismutase (SOD) in renal tissue were analyzed.Results Comparing with the sham group,ATO treatment reduced the elevation of BUN (mmol/L) (78.59±10.47 vs.128.54 ±6.69) andCr(μmol/L) (19.44±9.3vs.31.44±9.87) level,inhibited the expression of MPO (U/g) (1.25 ±0.14 vs.1.68 ±0.12),but increased the expression of SOD [U/(mg·pro)] (139 ± 10.6 vs.109 ±4.7),and enhance the elevation of NO (μmol/L)(94.65 ± 10.33 vs.67.50 ±8.32) and eNOS.All differences were significant.(P ＜0.01).Conclusion These data suggest that ATO protect renal function from ischemia-reperfusion injury probably by promote the expression of eNOS and consequently increase the production of NO. Key words: Atorvastatin preconditioning;  Ischemia/reperfusion;  Endothelial nitric oxide synthase;  Nitric oxide