Objective：This study aims to investigate the effects of sodium tanshinone type ⅡA sulphonate（STS）on lipopolysaccharide（LPS）-induced dysfunction and apoptosis of human umbilical vein endothelial cells（HUVEC）. Methods：Cultured HUVEC of 6-8 generation were grouped and stimulated as follows：DMEM group，LPS（1.0 μg/mL） group，high concentration（50.0 μg/mL）STS pre-treated group，medium concentration（25.0 μg/mL）STS pre-treated group，low concentration（12.5 μg/mL） STS pre-treated group. For STS pre-treated groups，HUVEC were pre-treated with corresponding concentrations of STS for 2 h，followed by the stimulation with 1 μg/mL LPS. After 24 h stimulation，cell viability was determined by CCK-8 method. Cell proliferation was detected by flow cytometry. Protein level of inflammatory cytokine interleukin-1 beta（IL-1β） in culture supernatant was determined by ELISA. Western blotting was employed for the detection of protein levels of intracellular IL-1β，cleaved caspase-3 and cleaved caspase-9，and nucleus-translocated nuclear factor-κB-p65（NF-κB-p65）. Then，migration ability of HUVEC was investigated by wound-healing test. The changes of cell and chromatin morphology in HUVEC were observed by microscopy，and the apoptosis of HUVEC was detected by Annexin V/PI staining. Results：Compared with DMEM，LPS treatment reduced viability and migration capacity of HUVEC，whereas promoted their proliferation. The protein levels of IL-1β，NF-κB-p65，cleaved caspase-3 and cleaved caspase-9 in HUVEC，as well as their apoptosis level were increased after LPS stimulation（P < 0.05）. However，STS can partially reverse the described effects of LPS in a dose-dependent manner（P < 0.05）. Conclusion：STS inhibits LPS-induced dysfunction and apoptosis in HUVEC，thus exerts protective effects on vascular endothelium.