Tea Polysaccharides Ameliorates Non-Alcoholic Fatty Liver Disease in Mice via Regulating Macrophages Polarization by Gut Microbial Metabolites

脂肪肝 脂质代谢 肝损伤 巨噬细胞极化 发病机制 炎症 新陈代谢 巨噬细胞 肝病 生物 疾病 丁酸 慢性肝病 内分泌学 内科学 非酒精性脂肪肝 化学 医学 多糖 药理学 细胞 免疫学 肝细胞 脂肪酸代谢 生物化学 库普弗电池 肠道菌群 促炎细胞因子
作者
Daixin Liu,Ang Li,Ping Li
出处
期刊:Current Issues in Molecular Biology [Caister Academic Press]
卷期号:48 (3): 338-338
标识
DOI:10.3390/cimb48030338
摘要

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and a global public health concern, for which there is currently no effective method to inhibit its progression. The pathogenesis of NAFLD is related to hepatic lipid metabolism disorders and liver inflammation. Previous studies have shown that tea polysaccharides (TPS) have the ability to regulate lipid metabolism and control inflammation. This study aimed to observe the effect of TPS on ameliorating NAFLD in a mouse model and to reveal its underlying mechanisms. In the current study, male C57BL/6J mice were fed a high-fat diet and administered 100 mg/kg TPS daily by gavage for 14 weeks. Then, liver injury indicators and macrophage polarization markers were detected. The results revealed that TPS could significantly ameliorate the progression of NAFLD and decrease liver injury indicators. Moreover, we found that treatment of NAFLD model mice with TPS could skew liver macrophages polarization from M1 to M2 type, which inhibited pro-inflammatory cytokines production and liver inflammation. Mechanistically, TPS cannot directly regulate the polarization of liver macrophages, but instead promotes the production of butyric acid by gut microbiota, which in turn regulates macrophage polarization. These findings suggest that TPS ameliorates NAFLD-associated inflammation by modulating the gut–liver axis and promoting M2 macrophage polarization, laying the foundation for the potential of TPS in the development of health foods for NAFLD.
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