Objective To investigate the effect and mechanism of evolocumab on hydrogen peroxide (H2O2)-induced oxidative damage in vascular endothelial cells. Methods Human umbilical vein endothelial cells (HUVECs) were cultured in vitro. According to previous research using H2O2 (700μmol/L) to establish oxidative stress injury model. The cells were pre-incubated with three dosages of evolocumab (25, 50 and 100 μmol/L) 0.5 h before exposure to H2O2. The cells were divided into control group, H2O2 group, H2O2+25 μmol/L evolocumab group, H2O2+50 μmol/L evolocumab group and H2O2+100 μmol/L evolocumab group. The cell viability was detected by MTS assay, intracellular reactive oxygen species (ROS) level and mitochondrial membrane potential (MMP) were measured using flow cytometry, apoptotic cells were detected using Hoechst 33258. Western blot was used to detect the protein expression level of Caspase-3, and malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor-α (TNF-α) and nterleukin-6 (IL-6) levels were measured using enzyme-linked immunosorbent assay (ELISA). Results Compared with the control group, the intracellular ROS, MDA, TNF-α and IL-6 levels in the H2O2 group increased, while the NO level decreased, accompanied by a decrease in MMP, the protein expression of Caspase-3 upregulation, and cell apoptosis. However, adding evolocumab before exposure to H2O2 could alleviate the decrease of cell viability caused by H2O/2, and the high dosage (100 μmol/L) of evolocumab had better effect. Further more, this study found that evolocumab could inhibit the production of ROS and MDA, and inhibit the increase of TNF-α and IL-6 levels. In addition, the addition of evolocumab could alleviate the decrease of NO level, inhibit the decrease in MMP, inhibit the protein expression of Caspase-3 upregulation and cell apoptosis. Conclusion Evolocumab alleviates the oxidative damage of vascular endothelial cells caused by H2O2 by antioxidation, inhibiting inflammation and apoptosis, and increasing the NO level