Effect Of Heat Shock Protein27, Erythropoietin And Heme Oxygenase-1Activated By Remote Ischemic Preconditioning On Kidney Ischemia/Reperfusion Injury

Objective:Observed the influence of the heat shock protein(HSP27)^erythropoietin(EPO) and heme oxygenase (HO-1) activation by remote ischemic preconditioning and how to protect kidney ischemia/reperfusion injury.Methods:90Male C57BL/6mice were randomly divided into three groups:I/R(n=30),IPC(IP+I/R)(n=30),Sham group(n=30).I/R group were subjected to ischemia25min and reperfusion24h; preconditioning group were subjected to bilateral renal ischemia20min and were exposed to I/R surgery on day8.Abdominal aortic blood was taken to test kidney function(Cr, BUN). Mice kidney specimens were sacrificed to expose to MPO staining of neutrophils infiltration、PAS staining to understand pathological changes、TUNEL staining to counting the number of apoptotic cells in the kidney of each group、Real-time PCR detection of kidney tissue to observe HSP27、EPO、HO-1mRNA expression. Results:Serum creatinine and blood urea nitrogen of IPC group and the Sham group were significantly lower than the I/R group (P<0.01);MPO staining found a large number of neutrophils in I/R group kidney(P<0.01);PAS staining showed that the kidney histopathology of IPC group was better than the I/R group (P<0.05);TUNEL staining analysis displayed that the apoptosis cells in IPC and Sham group were significantly less than in the I/R group (P<0.01); HSP27mRNA expression in IPC group was significantly higher than I/R and Sham group(P<0.01), the peak of expression of HSP27mRNA was at the eighth day. EPO、HO-1mRNA increased to A piont during24and48hours,and then decreased,but it was taken to another peak piont B at the eighth day and B was more higher than A.Conclusion:Remote ischemic preconditioning activated HSP27、EPO HO-1mRNA expression, taken part in reducing infiltration of inflammatory cytokines,promoted the repair and inhibition of tubular cell apoptosis, which protected the kidney ischemia-reperfusion injury.