# Asiaticoside promotes intestinal epithelial proliferation and barrier function in ischemia/reperfusion injury by activating FoxM1

## TL;DR

Asiaticoside helps repair intestinal damage from ischemia/reperfusion injury by boosting cell growth and barrier function through FoxM1 activation.

## Contribution

This study reveals that asiaticoside promotes intestinal recovery by activating FoxM1, a novel mechanism for treating II/R injury.

## Key findings

- Asiaticoside reduces the intestinal Chiu score and improves barrier protein expression after II/R injury.
- AS increases PCNA and Ki-67 expression, indicating enhanced cell proliferation in injured intestines.
- FoxM1 activation by AS is essential for its protective effects, as shown by reversal with a FoxM1 inhibitor.

## Abstract

The most important component of intestinal ischemia/reperfusion (II/R) injury is damage to the intestinal mucosal barrier. In II/R injury, damage and restoration occur simultaneously. To develop a treatment for II/R injury, further knowledge about the restoration of intestinal barrier function is needed. Whether asiaticoside (AS) has positive effects on barrier function following II/R injury is unclear, although multiple studies have reported that AS enhances intestinal recovery after injury. In our study, we discovered that AS can reduce the intestinal Chiu score after II/R injury (P < 0.05), increase intestinal barrier-associated protein expression (P < 0.05) and increase PCNA and Ki-67 expression after II/R injury (P < 0.05). Furthermore, following II/R injury, AS primarily activates FoxM1 expression, which promotes cell proliferation and enhances barrier function. TST (a FoxM1 inhibitor) administration significantly reversed the upregulation of FoxM1, as well as the intestinal epithelial proliferation and barrier function induced by AS pretreatment in rats after II/R injury. Therefore, our results reveal that AS promotes cell proliferation and barrier function by activating FoxM1 expression. Our findings may provide a new potential therapeutic approach for treating II/R injury with AS.