Curcumin improves the function of umbilical vein endothelial cells by inhibiting H(2)O(2)-induced pyroptosis

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 H(2)O(2)-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 H(2)O(2) and the optimal concentrations and time of curcumin to achieve therapeutic effects were explored. Curcumin was observed to inhibit H(2)O(2)-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.