〔Abstract〕 Objective To investigate the role of n-acetylcysteine(NAC) in lipopolysaccharide(LPS)-induced apoptosis of vascular endothelial cells, and to explore the possible mechanisms. Methods HUVECs were cultured in vitro and the apoptosis model of human umbilical vein endothelial cells was induced by LPS. Various concentrations of NAC were used to stimulate cells,and cell viability was assessed using the Cell Counting Kit-8( CCK-8) assay.Experiments were separated into four groups: control group,LPS group,NAC group,NAC and LPS group. Apoptosis rate was determined by using flow cytometry; The expression levels of Caspase-3,Bax,and Bcl-2 mRNA were determined by using real-time quantitative polymerase chain reaction( qRT-PCR); the expressions of Bcl-2,Bax,Caspase-3,p-p38 MAPK,and t-p38 MAPK proteins were determined by Western blotting. Results Compared with the control group,the cell viability of HUVECs decreased significantly,the apoptosis rate increased,downregulate the expression of Bcl-2,the expression of Bax,Caspase-3 were up-regulated,and upregulate the expression of phosphorylated p38 MAPK protein in the LPS group. However,these effects were inhibited by pretreatment with NAC.Conclusion NAC inhibits LPS-induced apoptosis of HUVECs through inhibiting the activity of p38 MAPK.