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Atherosclerosis‑induced cardiovascular diseases (CVDs) are accompanied by substantial morbidity and mortality. The loss and injury of endothelial cells is the primary cause of atherosclerosis. Rosuvastatin is an alternative agent used to reduce the risk of cardiovascular disease. Subsequently, the present study aimed to investigate the protective effects of rosuvastatin on oxidized‑low‑density lipoprotein (ox‑LDL)‑induced human umbilical vein endothelial cell (HUVEC) injury. The viability of ox‑LDL‑cultured HUVECs with or without rosuvastatin (0.01, 0.1 and 1 µmol/l) pretreatment, and pretreatment at different time points (3, 6, 12 and 24 h) was determined using an MTT assay. Morphological changes and the extent of apoptosis were detected; the anti‑oxidase activity, including superoxide dismutase (SOD) and catalase (CAT), was examined, and the contents of malondiahdehyde (MDA) and nitric oxide (NO) were measured. The phosphorylation levels of endothelial nitric oxide synthase (eNOS), protein kinase B (Akt) and phosphoinositide 3 kinase (PI3K) were detected using western blot analysis. The results demonstrated that pretreatment with 0.01‑1 µmol/l rosuvastatin decreased cell apoptosis caused by ox‑LDL. Notably, pretreatment with 1 µmol/l rosuvastatin for &gt;12 h increased cell viability. Additionally, DAPI staining revealed that rosuvastatin inhibited HUVEC apoptosis. Rosuvastatin treatment also resulted in increased SOD and CAT activities and decreased MDA content in ox‑LDL‑stimulated HUVECs. Furthermore, pretreatment with 0.01‑1 µmol/l rosuvastatin significantly increased` the NO content compared with HUVECs treated with ox‑LDL alone. Western blot analyses demonstrated that rosuvastatin upregulated the phosphorylation of eNOS, Akt and PI3K. These findings indicated that rosuvastatin could protect HUVECs against ox‑LDL‑induced injury through its anti‑oxidant effect and its ability to upregulate the expression of vascular endotheliocyte‑protecting factors.

Rosuvastatin protects against oxidized low‑density lipoprotein‑induced endothelial cell injury of atherosclerosis in�vitro