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
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI