Injury of vascular endothelial cell is one of the main factors triggering atherosclerosis. Peptide AAGALPS was derived from digestion and absorption product of rice α‐globulin, which was proved to prevent atherosclerosis in previous study. This study aims to investigate the potential effects of AAGALPS on improving tumor necrosis factor‐α (TNF‐α)‐stimulated human umbilical vein endothelial cells’ (HUVECs) injury. As a result, the viability of HUVECs stimulated by tumor necrosis factor‐α was significantly increased by AAGALPS in a dose‐dependent manner until 25?μg/ml. The peptide obviously reduced the levels of intercellular adhesion molecule‐1, vascular cell adhesion molecule‐1, nitric oxide, inducible nitric oxide synthase, reactive oxygen species, and malondialdehyde and increased the concentrations of glutathione peroxidase. Furthermore, AAGALPS inhibited the nuclear factor κB (NF‐κB) activation and nuclear translocation through regulating inhibitor of nuclear factor κB kinase α and inhibitor of NF‐κB. These results indicated that AAGALPS protected vascular endothelial cells through mediating inflammation and oxidative stress.
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