Aim To explore the mechanism of anoxia-reoxygenation injury (H/R) and the late protective effect of cato pril on endothelial cells (EC) . Methods To establish anoxia-reoxygenation model on human unbilical veins endothelial cell line ECV304, and observe the injury degree of anoxia and reoxygenationg at the different time. Then these ECs were randomly divided into 5 groups: catopril, catopril + bradykinin β₂ receptor inhibitor, catopril + PKC inhibitor, catopril + NOS inhibitor, catopril + NF-κB inhibitor, and obsene the cell morphologic changes, mortality and the activities of malondialdehyde (MDA), su peroxide dismutase (SOD), glutathione peroxidase (GSH-PX) . Results After treatment with anoxia and anoxia-reoxygen-ation, the ECs' morphologic changes were observed. The mortality increased and MDA concentration became higher, the concentration of SOD and CSH-PX became lower( P< 0.01). Meanwhile, the changes became more obviously with the time extending. The late preconditioning with catopril, the cell morphologic, MDA, SOD and CSH-PX keep normal. The protective effect became strenghen along with the catopril concentration increasing. However, culturing with above four inhibitors, the protective effect was partly diminished. Conclusion Anoxia and anoxia-reperfusion induce lipid peroxidation and the weakening of an tioxidation ability in a time-dependented manner. The late preconditioning with catopril can weaken anoxia-reperfusion injury in a concentration- dependented manner. Bradykinin β₂ receptor, PKC activating, nitric oxide and nucleus factor are all involved in the protective effect.