# Curcumin Protected CoCl2 ‐Induced Apoptosis and Ferroptosis in Human Umbilical Vein Endothelial Cells by Regulating the Expression of HSPA6

## TL;DR

Curcumin protects human umbilical vein endothelial cells from hypoxia-induced damage by regulating HSPA6 and reducing apoptosis and ferroptosis.

## Contribution

This study reveals a novel protective mechanism of curcumin in endothelial cells via downregulation of HSPA6 under hypoxic conditions.

## Key findings

- Curcumin reduces MMP1 and MMP13 expression while increasing TIMP-1 in hypoxia-induced HUVECs.
- Curcumin inhibits apoptosis, ferroptosis, and mitochondrial damage in HUVECs by downregulating HSPA6.
- Curcumin shows potential for treating hypoxia-induced vascular diseases like cardiovascular disorders.

## Abstract

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
Curcuma longa
, 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.

Curcumin reduces the expression of MMP1 and MMP13 while increasing TIMP‐1 levels by downregulating HSPA6 in CoCl2‐induced HUVECs. This mechanism attenuates apoptosis, ferroptosis, and mitochondrial damage in HUVECs. These findings suggest that curcumin holds promise for the clinical treatment of hypoxia‐induced vascular diseases.