Endothelial cell (EC) dysfunction is one of the initiating factors of atherosclerosis. EC dysfunction is primarily caused by oxidative damage and inflammation. As a classic non‑specific antioxidant and anti‑inflammatory drug, curcumin has been widely used in studies of lipid metabolism disorders. However, whether curcumin is able to alleviate H2O2‑induced EC damage and its related mechanisms has remained to be elucidated. The present study confirmed the protective effects of curcumin on human umbilical vein endothelial cells (HUVECs). A HUVEC injury model was established using H2O2 and the optimal concentrations and time of curcumin to achieve therapeutic effects were explored. Curcumin was observed to inhibit H2O2‑induced pyroptosis by inhibiting the activation of NOD‑, LRR‑ and pyrin domain‑containing protein 3. In addition, curcumin improved HUVEC function by restoring αvβ3 and reducing endothelin‑1 expression. In conclusion, the results of the present study revealed the mechanism through which curcumin inhibits pyroptosis and indicated that curcumin may have a potential utility in treating diseases of EC dysfunction.
Keywords: atherosclerosis; curcumin; endothelial cell; hydrogen peroxide; pyroptosis.