Effect Of Omi/HtrA2 Inhibitor On Tubular Cell Apoptosis Induced By Renal Ischemia-Reperfusion Injury In Rats

Objective To investigate the effect of Omi/HtrA2 inhibitor on tubular cell apoptosis induced by renal ischemia-reperfusion injury in rats .Method Male wistar rats were randomly divided into the following five groups: sham group(DMSO),model 1 group(I/R+DMSO before reperfusion), model 2 group (I/R+DMSO after reperfusion), treat 1 group(I/R+UCF101 before reperfusion) and treat 2 group(I/R+UCF101 after reperfusion). Renal ischemia/reperfusion injury(I/RI) model was made by clamping both renal arteries for 45 min Rats were sacrificed at 24h of reperfusion. The level of serum creatinine(SCr) and blood urea nitrogen(BUN) were measured by colorimetry; renal morphology changes were detected by periodic acid Schiff (PAS) stain; Tubular cell apoptosis was detected by terminal deoxynucleotidyl transferase(TDT)-mediated dUTP-biotin nick end labeling(TUNEL) assay;Protein expressions of renal caspase-3 and caspase-9 were detected by western blot.Result Renal I/R injury induced a significant increase of SCr and BUN(P<0.05) and changes of renal morphology(P<0.05) and apoptosis tubular cells(P<0.05) and increased protein expressions of caspase-3 and caspase-9(P<0.05). UCF-101 which was administered before 10 min reperfusion can markly improve renal function(P<0.05)and decreased tubular cell apoptosis(P<0.05) and the expressions of caspase-3 and caspase-9(P<0.05), while UCF-101 which was administered after 1h reperfusion can not alter renal morphology and renal function(P>0.05),tubular cell apoptosis(P>0.05) and the expressions of caspase-3 and caspase-9(P>0.05).Conclusion UCF-101 which was administered before 10 min reperfusion can suppress tubular cell apoptosis induced by renal I/R injury and protect renal function.