We aimed to investigate the role and mechanism of circ_0008896 in Atherosclerosis (AS) by using oxidized low-density lipoprotein (ox-LDL)-induced human aortic endothelial cell (HAECs). Levels of genes and proteins were measured by quantitative real-time PCR and Western blot. Functional experiments, including enzyme-linked immunosorbent assay analysis, cell counting kit-8, 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, tube formation assays and the detection of reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) generation, were performed to investigate the role of circ_0008896 on ox-LDL-induced HAEC damage. Circ_0008896 was increased in AS patients and ox-LDL-stimulated HAECs. Functionally, circ_0008896 knockdown reversed ox-LDL-induced inflammatory response, oxidative stress, apoptosis as well as arrest of proliferation and angiogenesis in HAECs in vitro. Mechanistically, circ_0008896 functioned as a sponge for miR-188-3p to relieve the repression of miR-188-3p on its target NOD2. A series of rescue experiments showed that miR-188-3p inhibition attenuated the protective effects of circ_0008896 knockdown on ox-LDL-stimulated HAECs, and NOD2 overexpression abolished the beneficial action of miR-188-3p in the suppression of inflammatory response and oxidative stress, and the promotion of cell growth and angiogenesis in HAECs under ox-LDL treatment. Circ_0008896 silencing attenuates ox-LDL-induced inflammatory response, oxidative stress, and growth arrest in HAECs in vitro, adding further understanding for the pathogenesis of AS.