Journal of ethnopharmacology · 2025
Dark tea ameliorates liver fibrosis via FXR/TGR5-mediated intestinal permeability and liver sinusoidal capillarization.
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Wang Chen-Yu, Liu Sen, Gao Chong, Dai Xu, Lian Li-Hua, Cui Zhen-Yu, Nan Ji-Xing, Wu Yan-Ling
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Dark tea, a post-fermented tea, has traditionally been used to regulate liver disorders. As an ethnomedicinal plant, its efficacy in alleviating chronic liver disease has been demonstrated.
AIM OF THE STUDY: This study explored the protective effect and potential mechanism of dark tea extract (DTE) against hepatic fibrosis.
MATERIALS AND METHODS: The chemical ingredients of DTE were analyzed by UPLC-MS, and active ingredients were identified using a multidimensional biomolecular assay. BALB/c mice were induced with thioacetamide (TAA) and then treated with DTE (100, 200, or 400 mg/kg) or curcumin. Hepatic stellate cells (HSCs) were stimulated with TGF-β or conditional medium from LPS-primed liver sinusoidal endothelial cells (LSECs), and then treated with DTE (50, 100, 200 μg/mL), GW4064, and Guggulsterones, respectively.
RESULTS: In vivo, DTE significantly reduced serum transaminase levels and collagen deposition, and alleviated liver and intestinal histopathological damage in TAA-induced mice. DTE upregulated the expression of farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5), inhibited inflammatory responses, and reduced intestinal permeability by regulating Occludin and ZO-1 expressions. Additionally, DTE regulated VEGFA, CD34 and LYVE1 expressions to improve hepatic sinusoidal capillarization. In vitro, DTE reversed HSCs activation by regulating extracellular matrix (ECM) accumulation, inflammation, and FXR-TGR5 expressions. Deficiency of FXR caused by an antagonist or siRNA blocked the regulation of DTE on ECM accumulation and inflammation. DTE downregulated CD34 and upregulated LYVE1 expressions, suppressed capillarization of LSECs and restored their differentiated phenotype. DTE further reversed activated HSCs stimulated by LSECs capillarization, which was related to the activation of FXR and TGR5.
CONCLUSIONS: DTE improves liver fibrosis by regulating collagen deposition, inflammation, intestinal permeability, and liver sinusoidal capillarization, which is a process closely related to FXR/TGR5.
AIM OF THE STUDY: This study explored the protective effect and potential mechanism of dark tea extract (DTE) against hepatic fibrosis.
MATERIALS AND METHODS: The chemical ingredients of DTE were analyzed by UPLC-MS, and active ingredients were identified using a multidimensional biomolecular assay. BALB/c mice were induced with thioacetamide (TAA) and then treated with DTE (100, 200, or 400 mg/kg) or curcumin. Hepatic stellate cells (HSCs) were stimulated with TGF-β or conditional medium from LPS-primed liver sinusoidal endothelial cells (LSECs), and then treated with DTE (50, 100, 200 μg/mL), GW4064, and Guggulsterones, respectively.
RESULTS: In vivo, DTE significantly reduced serum transaminase levels and collagen deposition, and alleviated liver and intestinal histopathological damage in TAA-induced mice. DTE upregulated the expression of farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5), inhibited inflammatory responses, and reduced intestinal permeability by regulating Occludin and ZO-1 expressions. Additionally, DTE regulated VEGFA, CD34 and LYVE1 expressions to improve hepatic sinusoidal capillarization. In vitro, DTE reversed HSCs activation by regulating extracellular matrix (ECM) accumulation, inflammation, and FXR-TGR5 expressions. Deficiency of FXR caused by an antagonist or siRNA blocked the regulation of DTE on ECM accumulation and inflammation. DTE downregulated CD34 and upregulated LYVE1 expressions, suppressed capillarization of LSECs and restored their differentiated phenotype. DTE further reversed activated HSCs stimulated by LSECs capillarization, which was related to the activation of FXR and TGR5.
CONCLUSIONS: DTE improves liver fibrosis by regulating collagen deposition, inflammation, intestinal permeability, and liver sinusoidal capillarization, which is a process closely related to FXR/TGR5.