Objective:To investigate the effects of intra-myocardial transfer of bradykinin (BK)preconditioning(PC)endothelial progenitor cells (EPCs)in a mouse model of acute myocardial infarction. Methods:Cells were divided into three groups:human EPCs(hEPCs)without BK preconditioning group(EPCs group),BK PC hEPCs group(BK PC group),BK PC hEPCs + HOE140(icatibant)group (BK PC/HOE group). In vitro,proliferative ability was detected by MTT assay. Apoptosis induced by hypoxia was determined by annexin V-fluorescein isothiocyanate/propidium iodide staining and Hoechst 33342 staining. Cytokine concentrations in supernatant were measured. In vivo,hEPCs was labeled with carbocyanine near-infrared dye DiD prior to heart transplantation. Nude mice were allocated to the following treatment groups:sham group,MI + saline group (placebo group),MI + hEPCs group(EPCs group),MI + BK PC hEPCs group(BK PC group),MI + BK PC hEPCs + HOE140 group(BK PC/HOE group). Cardiac function was evaluated by echocardiography and postmortem analysis were assessed 10 days after transplantation. Results:In vitro,BK PC significanty promoted EPCs proliferation compared with the EPCs group(P < 0.01). Cell apoptosis rate post hypoxia was significantly reduced in the BK PC group compared with that in the EPCs group(P < 0.01),and was blocked by HOE140(P < 0.01). VEGF level was also significantly up-regulated in the BK PC group compared with that in the EPCs group(P < 0.01),and was also blocked by HOE140(P < 0.01). The BK PC group showed robust cell apoptosis inhibition,infarct size reduction,and cardiac function improvement in vivo and these effects were abrogated by the HOE140. Conclusion:Efficacy of BK PC hEPCs on improving cardiac function was greater than those by hEPCs in the mouse ischemia model. Its therapeutic effect could be achieved by promoting cell survival and resisting transplanted cells and host cardiomyocytes apoptosis.