Lacticaseibacillus paracasei DCRFF018 improves alcoholic liver injury in mice by regulating gut microbiota and maintaining intestinal barrier

Alcoholic liver disease (ALD) poses a serious threat to public health. Although Lacticaseibacillus paracasei has been shown to mitigate symptoms of ALD, the mechanisms underlying these benefits have yet to be fully elucidated. The purpose of this study was to investigate both the effects and mechanisms of Lacticaseibacillus paracasei DCRFF018 (LP. DCRFF018) on alcohol-induced liver injury. The findings revealed that LP. DCRFF018 administration improved body weight, liver index, and liver function in alcohol-treated mice. Furthermore, LP. DCRFF018 inhibited hepatic lipid accumulation and inflammation by regulating the TLR4/NF-κB, AMPK/SREBP-1, and PPARα signaling pathways. By modulating the TLR4/NF-κB pathway and enhancing tight junction protein expression, LP. DCRFF018 alleviated colonic inflammation and preserved gut barrier integrity. Moreover, supplementing with LP. DCRFF018 regulated the structure and composition of gut microbiota. Notably, supplementation with LP. DCRFF018 significantly increased the relative abundance of Verrucomicrobiota and Akkermansia in alcohol-treated mice, while reducing the relative abundance of norank_f__Oscillospiraceae. Collectively, these findings demonstrate that LP. DCRFF018 improves alcoholic liver injury by regulating the gut microbiota and preserving intestinal barrier function, providing new insights into the management of ALD.