Stachydrine is a major constituent of Chinese herb leonurus heterophyllus sweet, which is used in clinics to promote blood circulation and dispel blood stasis. Our study aimed to investigate the role of stachydrine in human umbilical vein endothelial cells (HUVECs) injury induced by anoxia-reoxygenation. Cultured HUVECs were divided randomly into control group, anoxia-reoxygenation (A/R) group and 4 A/R+stachydrine groups. HUVECs in the control group were exposed to normoxia for 5 hours, while in all A/R groups, HUVECs underwent 3 hours anoxia followed by 2 hours reoxygenation, and HUVECs in the 4 A/R+stachydrine groups were treated with 10(-8) M, 10(-7) M, 10(-6) M and 10(-5) M (final concentration) of stachydrine respectively. After anoxia-reoxygenation, tissue factor (TF) was over-expressed, cell viability and the concentrations of SOD, GSH-PX and NO were declined, while LDH, MDA and ET-1 were over-produced (p < 0.05 to 0.001 vs. the control group). However, in stachydrine treated groups, TF expression was inhibited at both mRNA and protein levels, while the declined cell viability and SOD, GSH-PX, NO as well as the enhanced LDH, MDA and ET-1 levels occurred during anoxia-reoxygenation were ameliorated and reversed effectively (p < 0.05 to 0.01 versus A/R group). Consequently, our findings indicate that TF plays an important role in the development of anoxia-reoxygenation injury of HUVECs, stachydrine ameliorates HUVECs injury induced by anoxia-reoxygenation and its putative mechanisms are related to inhibition of TF expression.