Objective：This study aims to explore the role and mechanism of endothelial progenitor cells（EPC） promoting monocyte/macrophage to type M1 polarization under ischemia and reperfusion. Methods：the peripheral blood of healthy volunteers was obtained，the primary EPC and mononuclear/macrophage were cultured. The model of cell ischemia-reperfusion injury was established in vitro，and the expression of intercellular adhesion molecule -1（ICAM-1），vascular cell adhesion molecule -1（VCAM-1）and E- selectin on EPC surface were detected by flow cytometry. ELISA was used to detect the concentration of ICAM-1，VCAM-1 and E- selectin in the supernatant. Co-culture of EPC and mononuclear/macrophages was performed by Transwell chamber，and the ratio of M1 to M2 type monocytes/macrophages was detected by flow cytometry. Results：There was no significant change in the expression and the secretion of ICAM-1 and VCAM-1 of EPC under the ischemic reperfusion condition，and there was no significant difference between the two groups. The average fluorescence intensity of E- selectin on the surface of EPC was 10.89 in the control group and 33.93 in the ischemia reperfusion group（t=3.895，P=0.018）. The concentration of E- selectin in the EPC supernatant was 3.69 ng/mL in the control group and 18.17 ng/mL in the ischemia-reperfusion group（t=4.568，P=0.010）. Under ischemia reperfusion condition，EPC promoted monocyte/macrophage to M1 type polarization. The proportion of monocyte/macrophage type M1 was 58.83% in control group and was 81.43% in ischemia reperfusion group（t=5.394，P=0.006），E- selectin blockage could inhibit this effect（t=5.950，P=0.004）. Under ischemia reperfusion condition，EPC inhibited monocyte/macrophage to M2 type polarization. The ratio of M2 monocyte/macrophage was 60.57% in control group and was 35.30% in ischemia reperfusion group（t=6.424，P=0.003），E- selectin blockage could inhibit this effect（t=4.179，P=0.014）. Conclusion：Under the condition of ischemia-reperfusion injury，EPC can promote the monocyte/macrophage to M1 polarization through the high expression and secretion of E- selectin. Our research provides a new target for the treatment of ischemia-reperfusion injury.