# Effects of curcumol on ferroptosis and tube forming ability of hepatic sinus endothelial cells

## TL;DR

This study shows that curcumol induces ferroptosis and inhibits angiogenesis in liver cells, which may help treat liver fibrosis.

## Contribution

The study identifies the P53-TFR1-FTH1 signaling axis as a novel target of curcumol in hepatic sinusoidal endothelial cells.

## Key findings

- Curcumol increases P53 and TFR1 protein expression while decreasing FTH1.
- Curcumol promotes ferroptosis and inhibits angiogenesis in liver cells.
- P53 knockout rescues curcumol-induced ferroptosis but not angiogenesis inhibition.

## Abstract

To explore the effects of curcumol on ferroptosis and angiogenesis of hepatic sinusoidal endothelial cells, further elucidate the molecular mechanism of curcumol against liver fibrosis, and provide new ideas for the prevention and treatment of chronic liver disease.

We used VEGF to construct pathological model group, and divided hepatic sinusoidal endothelial cells into blank group, model group, high, middle and low curcumol group. Ferroptosis and angiogenesis were detected by various cell molecular biology experiments.

Curcumol significantly inhibited the proliferation and migration of hepatic sinusoidal endothelial cells, significantly increased the expression of P53 and TFR1 protein, significantly decreased the expression of FTH1 protein, significantly promoted the occurrence of iron death, and significantly inhibited angiogenesis. When we knocked out p53, the effect of curcumol contributing to the onset of ferroptosis was rescued, while curcumol’s role in inhibiting angiogenesis was saved, which was the same effect as when we used Ferrostatin-1.

Curcumol targets the P53-TFR1-FTH1 signalling axis and induces massive deposition of iron ions in hepatic sinusoidal endothelial cells, leading to the onset of ferroptosis inhibiting hepatic angiogenesis, which may be one of the molecular mechanisms of its anti-hepatic fibrosis.