Rapid communications in mass spectrometry : RCM · 2026
Chishizhi Yuyuliang Decoction Ameliorates Ulcerative Colitis in Mice by Promoting Colonic Epithelial Mucosal Healing via the CAV1/FA Axis.
СтатьяНазвание и аннотация: Перевод в очереди
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Hong Xing, Wen Yuxin, Xiao Benjiang, Jiang Qi, Chen Meng, Chen Pengyu, Qian Rui, Wang Qiong, Li Jingjing, Huang Fang, Huang Zhuang, Han Lintao
Аннотация
OBJECTIVE: This study aimed to investigate the therapeutic mechanisms of CY in treating UC using an integrated metabolomics and proteomics approach.
METHODS: A murine UC model was induced using dextran sulfate sodium (DSS). The therapeutic efficacy of CY was evaluated via histological examination (H&E staining) of colon tissues to assess inflammation, epithelial necrosis, and crypt abscesses. Serum and colon tissues were collected for ELISA, immunofluorescence, Western blotting, metabolomics, and proteomics analyses. Additionally, an in vitro intestinal epithelial barrier model was established using LPS-induced Caco-2 cells. Cell viability, barrier function (TEER and FITC-Dextran permeability), cell damage (LDH), and inflammatory cytokine levels (IL-6 and IL-1β) were measured. The expression and distribution of tight junction proteins (ZO-1 and occludin) and signaling proteins (FAK, p-FAK, paxillin, and p-paxillin) were analyzed via immunofluorescence and Western blotting.
RESULTS: CY treatment significantly reduced the Disease Activity Index (DAI) and suppressed the levels of pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) in UC mice. Proteomic analysis identified Caveolin-1 (CAV1) and the focal adhesion pathway as key therapeutic targets and signaling pathways. Metabolomic profiling revealed 17 endogenous metabolites, highlighting tryptophan metabolism and butyrate metabolism as critical pathways. Furthermore, CY intervention modulated arachidonic acid and linoleic acid metabolism. Mechanistically, CY upregulated the expression of CAV1 and FAK while downregulating AKT and paxillin phosphorylation. In vitro experiments demonstrated that CY-containing serum restored the barrier function of LPS-induced Caco-2 cells by regulating FAK/paxillin phosphorylation, upregulating tight junction proteins, and mitigating inflammatory responses.
CONCLUSION: CY involvement in colonic mucosal healing attenuates inflammation and enhances intestinal barrier function in DSS-induced colitis, likely through the modulation of the CAV1/FA axis. These findings provide a theoretical basis for the clinical application of CY and offer novel insights for the development of therapeutic agents for UC.
METHODS: A murine UC model was induced using dextran sulfate sodium (DSS). The therapeutic efficacy of CY was evaluated via histological examination (H&E staining) of colon tissues to assess inflammation, epithelial necrosis, and crypt abscesses. Serum and colon tissues were collected for ELISA, immunofluorescence, Western blotting, metabolomics, and proteomics analyses. Additionally, an in vitro intestinal epithelial barrier model was established using LPS-induced Caco-2 cells. Cell viability, barrier function (TEER and FITC-Dextran permeability), cell damage (LDH), and inflammatory cytokine levels (IL-6 and IL-1β) were measured. The expression and distribution of tight junction proteins (ZO-1 and occludin) and signaling proteins (FAK, p-FAK, paxillin, and p-paxillin) were analyzed via immunofluorescence and Western blotting.
RESULTS: CY treatment significantly reduced the Disease Activity Index (DAI) and suppressed the levels of pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) in UC mice. Proteomic analysis identified Caveolin-1 (CAV1) and the focal adhesion pathway as key therapeutic targets and signaling pathways. Metabolomic profiling revealed 17 endogenous metabolites, highlighting tryptophan metabolism and butyrate metabolism as critical pathways. Furthermore, CY intervention modulated arachidonic acid and linoleic acid metabolism. Mechanistically, CY upregulated the expression of CAV1 and FAK while downregulating AKT and paxillin phosphorylation. In vitro experiments demonstrated that CY-containing serum restored the barrier function of LPS-induced Caco-2 cells by regulating FAK/paxillin phosphorylation, upregulating tight junction proteins, and mitigating inflammatory responses.
CONCLUSION: CY involvement in colonic mucosal healing attenuates inflammation and enhances intestinal barrier function in DSS-induced colitis, likely through the modulation of the CAV1/FA axis. These findings provide a theoretical basis for the clinical application of CY and offer novel insights for the development of therapeutic agents for UC.