Dihydromyricetin Attenuates CCl4-Induced Hepatic Injury in Mice by Modulating the Intestinal Flora and Enhancing Antioxidative and Anti-Inflammatory Responses

Dihydromyricetin (DHM) is a natural flavonoid with diverse biological functions, but its protective mechanisms against chemically induced liver injury require deeper exploration.Here, BALB/c mice were randomized into a normal control group (FCR), a CCl4 model group (FMR) and a DHM treatment group (FYR).We systematically evaluated liver weights, organ indices, histopathological features, serum biochemical markers, oxidative stress parameters, inflammatory cytokines, and gut microbiota composition to assess DHM's hepatoprotective effects.The results showed that CCl4 exposure significantly increased liver weight and the liver index (P<0.01),whereas DHM administration effectively reversed this hypertrophy (P<0.05).Histopathological analysis confirmed that DHM markedly rescued the structural disorganization of hepatic tissue caused by CCl4 while reducing necrosis and fibrosis.Functionally, DHM significantly decreased serum ALT and AST levels (P<0.01),upregulated hepatic SOD activity (P<0.01), lowered MDA content (P<0.01) and suppressed pro-inflammatory cytokines like TNF-α and IL-6 (P<0.01).Microbiome profiling indicated that DHM selectively promoted the proliferation of beneficial gut bacteria, particularly Muribaculum and Bifidobacterium.These findings demonstrate that DHM exerts its hepatoprotective effects by optimizing gut microbiota composition, mitigating oxidative stress, and quenching inflammatory responses, suggesting Muribaculum and Bifidobacterium are key microbial drivers of this protection.This study establishes a robust experimental foundation for understanding DHM's therapeutic mechanisms and supports developing microbiotatargeted strategies to treat liver injury.