Objective：To investigate the effect and mechanism of ticagrelor on endothelial injury induced by ox -LDL. Methods： ELISA method was used to detect the serum ET-1 and NO contents. Cell viability，proliferation and migration ability were determined by CCK-8，EdU kit and Transwell assay respectively. Annexin V-PI assay was used to detect cell apoptosis. The levels of DNMT1 and p16 were detected by Real-time PCR and Western blot. The lentiviral overexpression vector pLVX-puro-EGFP was used to construct the p16 overexpression system. The lentiviral knockout vector pLKO.1 was used to construct the DNMT1 and p16 knockout system. The methylation status of p16 promoter region was determined by the methylation-specific PCR method. Results：Ticagrelor promoted the viability，proliferation and migration ability of human umbilical endothelial cell(HUVEC)treated with ox-LDL，and significantly inhibited ox - LDL - induced apoptosis. Ticagrelor down - regulated the expression of p16 in HUVECs induced by ox - LDL，and overexpressed p16 could reverse the protective effect of ticagrelor on HUVECs induced by ox-LDL. DNMT1 inhibited the expression of p16 by affecting the methylation level of p16 promoter region. Conclusion：Ticagrelor could reduce the injury of HUVECs induced by ox-LDL and improve endothelial function. The mechanism might be related to the regulation of DNMT1/p16 signaling pathway.