The Effect Of Estrogen On Hypoxic Vascular Endothelial Cells And Its Secretions (tPA And PaI-1)

Objective: Although extensive evidence indicates that estrogen has the important protective role on the coronary artery disease, the mechanism through which estrogen might exert its protective effect has not been adequately explained. We simulated the condition of acute myocardial infarction (AMI),and investigated whether estrogen could protect hypoxic vascular endothelial cells and increase fibrinolytic activity in hypoxic vascular endothelial cells. Methods: Human umbilical vein endothelial cells (HUVEC) were incubated in vitro. The experiment consisted of five groups: hormoxia; hypoxia; hypoxia and treated with the different concentration of estrogen (10mol/L; 10-8mol/L; lO"'癿ol/L). Morphologic change of HUVEC and F-actin was observed. Cell viability was assessed . PAI-l and tPA antigen were detected by ELISA. Results: Hypoxia could induce the destruction of F-actin, decrease endothelial cell viability, and increase tPA, PAI-l antigen and tPA/PAI-l levels. Compared with the group of hypoxia, estrogen could increase hypoxic cell viability (PO.Ol) and probably relieve the impairment of F-actin in hypoxia HUVEC, increase tPA levels in hypoxic endothelial cells, and increase tPA/PAI-l level (PO.Ol). Conclusion : Hypoxia could injure the endothelial cells and stimulatethe release of tPA and PAI-1. Estrogen could not only protect the hypoxic endothelial cell cytoskeleton and cell viability , but also increase fibrinolytic activity and facilitate spontaneous thrombolysis. This may be one of the mechanisms that estrogen protect patients with AMI.Lei jun (Cardiovasology)Director by Professor Cai shanglang...