In this study, we investigated the ameliorative effects of selenium-enriched 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.
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