Protective effect of extracts against acute alcoholic liver injury via suppressing TLR/NF-κB signal pathway and modulating intestinal microbiota in mice.

Excessive alcohol consumption is leading to increased rates of liver injury and disease. A new research strategy focuses on manipulating gut microbiota to lessen alcohol-induced harm. This study examined the hepatoprotective effects of extracts from (EAI) on acute alcoholic liver injury by inhibiting the TLR/NF-κB signalling pathway and modulating intestinal microbiota in mice. The results showed that EAI dose-dependently reduced alcohol-induced elevations of AST, ALT, and ALP levels. EAI showed significant inhibitory effects on the expressions of TLR, NF-κB, and pNF-κB proteins. Furthermore, EAI caused a notable reduction in hepatic levels of IL-1β, IL-6, and TNF-α. Supplementation with EAI could ameliorate alcohol-induced dysbiosis of intestinal bacteria. The levels of ALT, AST, and ALP levels were negatively correlated with , , and , but positively correlated with and . Overall, EAI alleviated alcoholic liver injury in mice by inhibiting the TLR/NF-κB signalling pathway and modulating intestinal bacteria.