Curcumin Protected <scp> CoCl ₂ </scp> ‐Induced Apoptosis and Ferroptosis in Human Umbilical Vein Endothelial Cells by Regulating the Expression of <scp>HSPA6</scp>

Hypoxia-induced vascular endothelial cell (EC) injury is the main pathologic mechanism for the development of vascular diseases, such as venous thrombosis, heart disease, and cerebral obstruction. Curcumin, the main active component in the rhizome of <i>Curcuma longa</i>, has anti-inflammatory and antioxidant properties. The aim of the study was to elucidate the underlying mechanisms of curcumin's protective effects on endothelial cells. Cobalt chloride (CoCl₂) was used to induce hypoxia in human umbilical vein endothelial cells (HUVECs) in vitro, followed by treatment with curcumin. We found that curcumin can enhance cell proliferation, promote cell cycle progression, decrease MMP1 and MMP13 expression, and increase TIMP-1 expression in CoCl₂-induced HUVECs. Meanwhile, curcumin inhibits CoCl₂-induced apoptosis, ferroptosis, and mitochondrial damage in HUVECs. Further studies revealed that curcumin exerted endothelial cell protective effects by down-regulating HSPA6 expression. Curcumin exerts a vascular endothelial protective effect on hypoxia-induced apoptosis and mitochondrial damage in HUVECs. Thus, curcumin is very effective for the clinical treatment of hypoxia-induced vascular diseases, such as cardiovascular diseases, venous thrombosis, and so on.