Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Poricoic acid A alleviates dextran sulfate sodium-induced colitis in mice by regulating AMPK/mTOR-mediated autophagy and inhibiting intestinal epithelial cell apoptosis].
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Qiao Tong, Yin Lin, Zhang Keni, Niu Minzhu, Huang Ju, Geng Zhijun, Li Jing, Hu Jianguo
Аннотация
OBJECTIVES: 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.
CONCLUSIONS: PAA protects intestinal barrier function and alleviates DSS-induced colitis in mice by activating AMPK/mTOR-mediated autophagy and inhibiting intestinal epithelial cell apoptosis.
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.
CONCLUSIONS: PAA protects intestinal barrier function and alleviates DSS-induced colitis in mice by activating AMPK/mTOR-mediated autophagy and inhibiting intestinal epithelial cell apoptosis.