Poricoic acid A alleviates dextran sulfate sodium-induced colitis in mice by regulating AMPK/mTOR-mediated autophagy and inhibiting intestinal epithelial cell apoptosis
QIAO Tong
YIN Lin
ZHANG Keni
NIU Minzhu
HUANG Ju
Geng Zhijun
LI Jing
HU Jianguo
Abstract：Objective To investigate the mechanism of poricoic acid A(PAA)for alleviating dextran sulfate sodium(DSS)-induced colitis in mice.Methods Eighteen C57BL/6 mice were randomly divided into control group,DSS-induced colitis model group,and PAA intervention(10 mg/kg)group.The changes in body weight,colon length,disease activity index(DAI),and histopathological scores of the mice were evaluated.In a DSS-induced Caco-2 cell model,the changes in expressions of ZO-1,claudin-1,Bcl-2,Bax,cleaved caspase-3,LC3-II/I,and P62 were detected.Molecular docking and Western blotting were used to analyze the mechanisms underlying the ameliorating effect of PAA on DSS-induced colitis.Results In the mouse models of DSS-induced colitis,PAA significantly ameliorated DSS-induced weight loss,colon shortening,and elevation of DAI scores while reducing colonic IL-1β and TNF-α levels.HE staining showed that PAA obviously alleviated colonic crypt damage,reduced inflammatory cell infiltration,and lowered histopathological scores of the colon.AB-PAS staining revealed significantly increased goblet cell counts in PAA-treated mice compared to those in DSS group.In DSS-induced Caco-2 cells,PAA treatment effectively inhibited DSS-induced downregulation of the tight junction proteins,reduced Bax and cleaved caspase-3 expressions,increased Bcl-2 expression and the LC3-II/I ratio,and decreased P62 expression.Mechanistic study suggested that PAA targeted the AMPK/mTOR pathway to activate autophagy and suppress cell apoptosis.Conclusion PAA protects intestinal barrier function and alleviates DSS-induced colitis in mice by activating AMPK/mTOR-mediated autophagy and inhibiting intestinal epithelial cell apoptosis.
Keywords：inflammatory bowel diseaseporicoic acid Aautophagyapoptosisintestinal barrier
Publication Date：2026-01-20
Online Publishing Date：2026-01-22(First online date of this platform, not the publication date of the document)
Pages：10( 131-140 )