Effect And Mechanism Of Renal Progenitor Cells Induced By Ischemic Preconditioning On Ischemia-reperfusion Injury After Nephron Sparing Surgery

Background:Nephron sparing surgery is a promising therapy of renal cell carcinoma,however,ischemia-reperfusion injury during operation is the major factors influence prognosis.Ischemic preconditioning as a kind of endogenous protective mechanism could play a role in ischemia-reperfusion injury repair,also increase the SDF-1?CXCR7 expression at the same time.While CXCR7 and SDF-1 have been confirmed plays an important role for renal progenitor cells survive and proliferation.Objective:The objective of this study was to investigate the role of renal progenitor cells(RPCs)in the modulation of ischemia-reperfusion injury(IRI)in a nephron sparing surgery(NSS)rat model using ischemic preconditioning(IPC).Materials and methods:Fifty-four Sprague-Dawley rats were randomly divided into three groups following right-side nephrectomy:Sham-operated rats(surgery without vascular clamping);NSS rats(renal blood vessels were clamped for 40 min and NSS was performed);IPC rats(pretreated with 15 min ischemia and 10 min reperfusion).At 12 h,24 h,72 h after reperfusion,the blood samples and renal tissues were collected.The degree of renal injury was assessed,along with RPCs counts,stromal cell-derived factor 1,CXCR7 expression.Results:Rats with ischemic preconditioning after Nephron sparing surgery exhibited significant improvements in renal function and morphology.RPCs quantity in the kidney were increased at 24 h following reperfusion in the IPC group compared with the NSS or sham groups.In addition,stromal cell-derived factor 1(SDF-1)and CXCR7 expression were higher in IPC group than those in the NSS group.Conclusions:Ischemic preconditioning may attenuate renal IRI induced by NSS;RPCs could be mobilized by IPC,SDF-1 as well as CXCR7 in renal tissues may play key role in mobilized process of RPCs.