Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Verbenalin ameliorates intestinal inflammation and colitis in a mouse model of Crohn's disease by inhibiting the PI3K-AKT pathway].
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Huang Linlin, Zheng Wang, Hu Jianguo, Song Xue, Tao Lu, Geng Zhijun, Li Jing, Zuo Lugen, Ge Sitang
Аннотация
OBJECTIVES: To investigate the therapeutic effect of verbenalin (VE) on Crohn's disease (CD)‑like colitis and the underlying molecular mechanism.
METHODS: Fifty C57BL/6 mice were randomly divided into control group, TNBS group, and low-, medium-, and high-dose VE treatment groups (n=10). Mouse models of CD-like colitis were established in all but the control group by enema with 25 mg/L TNBS dissolved in ethanol, and the mice in VE treatment groups received daily intraperitoneal injections of VE at 5, 10, or 20 mg/kg for 7 days. Cultured colon organoids derived from mouse crypts were exposed to 100 μg/mL lipopolysaccharide (LPS) for 24 h and treated with 5, 10, or 20 μmol/L VE. The therapeutic effects of VE in the mouse models were evaluated by assessing changes in disease activity index (DAI), histopathological scores, and spleen index. In both colonic mucosa of the mouse models and the colon organoids, the levels of inflammatory cytokines, expressions of tight junction proteins, and changes in PI3K-AKT pathway proteins were analyzed, and the regulatory mechanism of VE was verified using the PI3K-AKT agonist 740 Y-P.
RESULTS: In TNBS-treated mice, VE treatment significantly reduced DAI, histopathological scores, and spleen index, and mitigated weight loss, colon shortening and bacterial translocation. VE obviously lowered the expression of pro-inflammatory cytokines in colonic mucosa of the mice and the colon organoids, upregulated ZO-1 and claudin-1 expressions, and reduced bacterial translocation. VE significantly downregulated p-PI3K and p-AKT protein expressions, which was reversed by treatment with 740 Y-P.
CONCLUSIONS: VE inhibits intestinal inflammation and protects intestinal barrier function in mice with CD-like colitis by modulating the PI3K-AKT signaling pathway.
METHODS: Fifty C57BL/6 mice were randomly divided into control group, TNBS group, and low-, medium-, and high-dose VE treatment groups (n=10). Mouse models of CD-like colitis were established in all but the control group by enema with 25 mg/L TNBS dissolved in ethanol, and the mice in VE treatment groups received daily intraperitoneal injections of VE at 5, 10, or 20 mg/kg for 7 days. Cultured colon organoids derived from mouse crypts were exposed to 100 μg/mL lipopolysaccharide (LPS) for 24 h and treated with 5, 10, or 20 μmol/L VE. The therapeutic effects of VE in the mouse models were evaluated by assessing changes in disease activity index (DAI), histopathological scores, and spleen index. In both colonic mucosa of the mouse models and the colon organoids, the levels of inflammatory cytokines, expressions of tight junction proteins, and changes in PI3K-AKT pathway proteins were analyzed, and the regulatory mechanism of VE was verified using the PI3K-AKT agonist 740 Y-P.
RESULTS: In TNBS-treated mice, VE treatment significantly reduced DAI, histopathological scores, and spleen index, and mitigated weight loss, colon shortening and bacterial translocation. VE obviously lowered the expression of pro-inflammatory cytokines in colonic mucosa of the mice and the colon organoids, upregulated ZO-1 and claudin-1 expressions, and reduced bacterial translocation. VE significantly downregulated p-PI3K and p-AKT protein expressions, which was reversed by treatment with 740 Y-P.
CONCLUSIONS: VE inhibits intestinal inflammation and protects intestinal barrier function in mice with CD-like colitis by modulating the PI3K-AKT signaling pathway.