In this study, we investigated the ameliorative effects of selenium-enriched Lactobacillus fermentum FZU3103 (Lf@Se) and its pathway on alcoholic liver injury (ALI) in mice. The results showed that Lf@Se was superior to Lf and inorganic selenium in alleviating ALI. Oral Lf@Se effectively prevented lipid metabolism disorders, improved liver function, promoted alcohol metabolism, and alleviated liver oxidative damage in mice. 16S amplicons sequencing indicated that Lf@Se intervention modulated intestinal flora homeostasis by increasing (decreasing) the abundance of beneficial bacteria (harmful bacteria), which is associated with the improvement of liver function. Besides, Lf@Se intervention altered the liver metabolic profile, and the characteristic biomarkers were mainly involved in tyrosine metabolism, retinol metabolism, galactose metabolism, and primary bile acid biosynthesis. Additionally, Lf@Se intervention regulated liver gene expression for lipid metabolism and oxidative stress. Western blot analysis revealed increased expression levels of intestinal tight junction proteins after Lf@Se intervention, thereby ameliorating alcohol-induced intestinal barrier damage.

中文翻译：

---

肠道微生物组学和肝脏代谢组学对富硒发酵乳杆菌FZU3103对酒精诱导的小鼠肝损伤的改善作用的见解


在本研究中，我们研究了富硒发酵乳杆菌 FZU3103 （Lf@Se） 及其通路对小鼠酒精性肝损伤 （ALI） 的改善作用。结果表明，Lf@Se 在缓解 ALI 方面优于 Lf 和无机硒。口服Lf@Se有效预防小鼠脂质代谢紊乱，改善肝功能，促进酒精代谢，减轻肝脏氧化损伤。16S 扩增子测序表明，Lf@Se干预通过增加（减少）有益菌 （有害菌） 的丰度来调节肠道菌群稳态，这与肝功能的改善有关。此外，Lf@Se干预改变了肝脏代谢特征，特征性生物标志物主要参与酪氨酸代谢、视黄醇代谢、半乳糖代谢和初级胆汁酸生物合成。此外，Lf@Se干预调节肝脏脂质代谢和氧化应激的基因表达。Western blot 分析显示，Lf@Se干预后肠道紧密连接蛋白的表达水平增加，从而改善酒精诱导的肠道屏障损伤。