Ethanol-Tolerant Lactobacillus rhamnosus L7 Ameliorates Alcohol-Induced Liver Injury in Mice by Inhibiting the TLR4/MyD88/NF-κB Inflammatory Signaling Pathway and Restoring Gut Microbiota Homeostasis.

Alcohol-related liver disease (ALD) represents a growing global public health concern, and there is still a lack of safe, effective clinical intervention approaches to date. This study aimed to evaluate the protective effect of ethanol-tolerant Lactobacillus (L.) rhamnosus L7 on ALD in mice. In this work, L. rhamnosus L7 with high ethanol tolerance was isolated from fermented grains and pit mud. The strain was intragastrically gavaged to mice with alcoholic liver injury established via the Gao-binge model using the Lieber-DeCarli ethanol liquid diet. Physiological symptoms, histopathological changes, oxidative stress indicators, inflammatory cytokines, gut microbiota composition and the expression of liver injury-related proteins were detected to evaluate the alleviative effect and potential mechanism of L. rhamnosus L7 on alcohol-induced liver injury. The results showed that supplementation with L. rhamnosus L7 significantly decreased serum alanine transaminase (ALT), aspartate transaminase (AST), total cholesterol (TC) and triglyceride (TG) levels. L. rhamnosus L7 intervention markedly alleviated alcohol-triggered hepatic injury, inhibited hepatic steatosis, and alleviated the degree of hepatocellular swelling. Moreover, L. rhamnosus L7 increased the levels of hepatic superoxide dismutase (SOD), catalase (CAT) and total antioxidant capacity (T-AOC), while suppressing the levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), thereby enhancing antioxidant defense and anti-inflammatory capacity. In addition, L. rhamnosus L7 effectively restored gut microbial homeostasis by regulating the structure of gut microbiota at both phylum and species levels. In conclusion, these findings indicate that L. rhamnosus L7 is expected to be developed as a functional probiotic preparation, providing a novel candidate strain and theoretical basis for the alleviation of ALD.