Auricularia auriculaPolysaccharides Exert Anti-inflammatory Effects in Hepatic Fibrosis by the Gut-Liver Axis and Enhancing SCFA Metabolism

被引:0
|
作者
Zhang, Lu [1 ]
Liu, Zhao-Xiu [1 ]
Liu, Yi-Heng [1 ]
Chen, Yuyan [2 ]
Chen, Jing [1 ]
Lu, Cui-Hua [1 ]
机构
[1] Department Gastroenterology, Medical School of Nantong University, Affiliated Hospital of Nantong University, Nantong,226001, China
[2] Division of Hepatobiliary and Transplantation Surgery, Department of General Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing,210008, China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
Fungi - Fungus protection - Medicinal chemistry - Physiological models;
D O I
10.1021/acs.jafc.4c07952
中图分类号
学科分类号
摘要
Auricularia auricula, esteemed in Chinese culture for their culinary and medicinal properties, exhibits notable metabolic and immunomodulatory effects. The principal active constituents are indigestible fermentable polysaccharides, which not only exhibit anti-inflammatory activities but also facilitate the proliferation of beneficial gut microbiota. However, the influence of gut-derived components on liver-regulated metabolic products remains insufficiently understood. This item offers insights into the therapeutic potential of wood ear mushrooms for treating hepatic fibrosis and the associated mechanisms. Following 8 weeks of treatment, a substantial reduction in ECM deposition was recorded, linked to modulation of the NLRP3 inflammasome activation. This study aims to reveal the potential microbiome-mediated mechanisms behind its therapeutic effects. Insights from antibiotic combination treatments indicate that the protective effects against ECM deposition rely on the presence of specific gut microbiota. This fecal microbiota intervention enhances key physiological mechanisms, underscoring the contributions of Lactobacillales, Rikenellaceae, and Bacteroidaceae in potentially mitigating fibrosis. Collectively, these findings suggest that interventions utilizing wood ear mushrooms may reduce inflammation and ECM deposition, mediated by the TLR4/NF-κB pathway. © 2025 The Authors. Published by American Chemical Society.
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收藏
页码:4617 / 4629
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