Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Ethyl caffeate alleviates dextran sulfate sodium-induced colitis in mice by restoring intestinal epithelial tight junctions via activating the Wnt/β-Catenin pathway].
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Zhang Keni, Zhang Longtao, Zhang Yu, Huang Ju, Li Qingqing, Geng Zhijun, Hu Jianguo, Li Jing
Аннотация
OBJECTIVES: To observe the effect of ethyl caffeate (EC) on intestinal barrier function in mice with dextran sulfate sodium (DSS)-induced murine colitis and explore the possible mechanism.
METHODS: Forty male C57BL/6 mice were randomized into control group, DSS model group, and 3 EC groups treated with EC at 5, 10, or 20 mg/kg. Mouse models of colitis were established bytreatment with 2.5% DSS for 7 days, and EC treatment was administered daily by gavage. Colitis phenotypes were assessed by changes in body weight, disease activity index (DAI), colon length and histology. Immunofluorescence staining and PAS staining were used to examine the changes in expressions of the tight junction proteins ZO-1 and claudin-1 and goblet cells, respectively. The intestinal levels of inflammatory factors were detected by ELISA, RT-qPCR and immunohistochemistry. Network pharmacology combined with Western blotting and Wnt inhibitor (IWR-1) was used to verify the mechanism of EC for ameliorating colitis.
RESULTS: Treatment with EC at 10 mg/kg significantly alleviated DSS-induced colitis in the mouse models, reduced intestinal pro-inflammatory cytokines and MPO levels, increased goblet cell counts, and restored ZO-1 and claudin-1 expressions and their membrane localization. Network pharmacology identified Wnt/β‑catenin and tight junction pathways as the core targets of EC, which activated the Wnt/β‑catenin pathway by upregulating WNT3A/β‑catenin, and this effect was blocked by treatment with IWR-1.
CONCLUSIONS: EC ameliorates DSS-induced colitis in mice by activating Wnt/β‑catenin signaling to restore tight junction protein expressions and localization, thereby improving intestinal barrier function, suggesting the value of EC as a novel candidate for treatment of inflammatory bowel disease.
METHODS: Forty male C57BL/6 mice were randomized into control group, DSS model group, and 3 EC groups treated with EC at 5, 10, or 20 mg/kg. Mouse models of colitis were established bytreatment with 2.5% DSS for 7 days, and EC treatment was administered daily by gavage. Colitis phenotypes were assessed by changes in body weight, disease activity index (DAI), colon length and histology. Immunofluorescence staining and PAS staining were used to examine the changes in expressions of the tight junction proteins ZO-1 and claudin-1 and goblet cells, respectively. The intestinal levels of inflammatory factors were detected by ELISA, RT-qPCR and immunohistochemistry. Network pharmacology combined with Western blotting and Wnt inhibitor (IWR-1) was used to verify the mechanism of EC for ameliorating colitis.
RESULTS: Treatment with EC at 10 mg/kg significantly alleviated DSS-induced colitis in the mouse models, reduced intestinal pro-inflammatory cytokines and MPO levels, increased goblet cell counts, and restored ZO-1 and claudin-1 expressions and their membrane localization. Network pharmacology identified Wnt/β‑catenin and tight junction pathways as the core targets of EC, which activated the Wnt/β‑catenin pathway by upregulating WNT3A/β‑catenin, and this effect was blocked by treatment with IWR-1.
CONCLUSIONS: EC ameliorates DSS-induced colitis in mice by activating Wnt/β‑catenin signaling to restore tight junction protein expressions and localization, thereby improving intestinal barrier function, suggesting the value of EC as a novel candidate for treatment of inflammatory bowel disease.