ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Integrative and Regenerative Pharmacology
Asiaticoside promotes intestinal epithelial proliferation and barrier function in ischemia/reperfusion injury by activating FoxM1
Provisionally accepted
- Central Hospital of Dalian University of Technology, Dalian, China
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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.
Keywords: AS, Barrier function, FoxM1, Intestinal ischemia/reperfusion injury, proliferation
Received: 07 Dec 2025; Accepted: 06 Feb 2026.
Copyright: © 2026 Zu, Zhao, Du, Wu and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Guo Zu
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