Objective: To investigate the effect and mechanism of Xuesaitong(XST) on the apoptosis of human umbilical vein endothelial cells (HUVEC) induced by hydrogen peroxide. Method: HUVECs were cultured in vitro and H2O2 was used as oxidants to establish oxidative stress model in HUVEC. The changes of apoptosis induced by H2O2 in HUVEC cells were observed by XST intervention

and the protective effect of XST on HUVEC was discussed from the perspective of epigenetic miRNA. The cultured HUVECs were divided into blank control group

H2O2 model group

and H2O2 model+XST (30 mg·L-1

24 h) group. The cell viability was detected by cell counting kit8 (CCK8) method; apoptosis was detected by Annexin V/Propidium iodide (PI); and the expression of miRNA-146 and miRNA-199 was detected by Real-time PCR. Result: After 100 μmol·L-1 H2O2 treatment

the late apoptosis and early apoptosis of HUVECs were significantly increased (P<0.05). Pretreatment of HUVEC cells with a dose of 1 mg·L-1 to 100 mg·L-1 showed that a significant improvement in cell proliferation was present in 10 mg·L-1 preconditioning. Apoptotic detection of Annexin V/PI double staining showed that the PI positive rate R3 (late apoptotic) and Annexin V positive rate R5 (early apoptosis) were significantly increased after HUVEC treatment with 100 μmol·L-1 H2O2 significantly (P<0.05). While the cell PI positive rate R3 (late apoptosis) and Annexin V positive rate R5 (early apoptosis) were significantly reduced after 30 mg·L-1 XST treatment in H2O2 models (P<0.05). The expression levels of hsa-miR-146b-5p and hsa-miR-199a-5p were significantly increased by H2O2 treatment at 100 μmol·L-1. As compared with H2O2 group

the expression of hsa-miR-146b-5p was significantly decreased after treatment with 30 mg·L-1 XST (P<0.05). Conclusion: XST can significantly resist H2O2-induced oxidative damage in HUVEC cells

which may play a protective role by inhibiting the increase of hsa-miR-146b-5p.