Gut microbiota (GM) dysbiosis and bile acid (BA) metabolism disorder play an important role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Probiotics had a beneficial effect on NAFLD, but further study is needed to explore probiotics as a potential therapeutic agent to NAFLD. The aim of this study was to investigate the regulatory effect of probiotics on gut microbiota in NAFLD rats and to explore the possible mechanism of probiotics regulating the bile acid receptor farnesoid X receptor/growth factor 15 (FXR/FGF15) signaling pathway in rats. We established a rat model of NAFLD fed with a high-fat diet (HFD) for 14 weeks, which was given different interventions (312 mg/kg/day probiotics or 10 mg/kg/day atorvastatin) from the 7^th week. Serum lipids and total bile acids (TBA) were biochemically determined; hepatic steatosis and lipid accumulation were evaluated with HE staining. The expression levels of FXR, FGF15 mRNA, and protein in rat liver were detected. 16S rDNA was used to detect the changes of gut microbiota in rats. Compared with the HFD group, probiotics and atorvastatin significantly reduced serum lipids and TBA levels. And probiotics increased dramatically the expression of FXR, FGF15 mRNA, and protein in the liver. But there were no significant changes in the atorvastatin group. Probiotics and atorvastatin can upregulate the diversity of gut microbiota and downregulate the abundance of pathogenic bacteria in NAFLD model rats. In summary, probiotics alleviated NAFLD in HFD rats via the gut microbiota/FXR/FGF15 signaling pathway.

中文翻译：

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益生菌通过肠道微生物群/FXR/FGF15 信号通路减轻高脂饮食喂养大鼠的非酒精性脂肪肝

肠道菌群 (GM) 生态失调和胆汁酸 (BA) 代谢紊乱在非酒精性脂肪性肝病 (NAFLD) 的发病机制中起重要作用。益生菌对 NAFLD 具有有益作用，但需要进一步研究以探索益生菌作为 NAFLD 的潜在治疗剂。本研究旨在探讨益生菌对NAFLD大鼠肠道菌群的调节作用，并探讨益生菌调节大鼠胆汁酸受体法尼醇X受体/生长因子15（FXR/FGF15）信号通路的可能机制。我们建立了高脂饮食（HFD）喂养 14 周的 NAFLD 大鼠模型，从第 7 天开始给予不同的干预措施（312 mg/kg/day 益生菌或 10 mg/kg/day 阿托伐他汀）^。星期。生化测定血清脂质和总胆汁酸（TBA）；用HE染色评估肝脂肪变性和脂质积累。检测大鼠肝脏中FXR、FGF15 mRNA和蛋白的表达水平。16S rDNA用于检测大鼠肠道菌群变化。与 HFD 组相比，益生菌和阿托伐他汀显着降低了血脂和 TBA 水平。益生菌显着增加了肝脏中 FXR、FGF15 mRNA 和蛋白质的表达。但阿托伐他汀组没有显着变化。益生菌和阿托伐他汀可上调NAFLD模型大鼠肠道菌群多样性，下调病原菌丰度。总之，益生菌通过肠道菌群/FXR/FGF15信号通路减轻了HFD大鼠的NAFLD。