Influence of Salvianolic Acid B on Liver Injury and Intestinal Bacteria in Mice Caused by Acute Alcohol Consumption

Background Alcoholic liver disease, a consequence of excessive alcohol consumption, is a major factor contributing to global morbidity and mortality. Salvianolic acid B (Sal B) has demonstrated potential in alleviating ethanol-induced hepatic damage; however, the precise mechanisms, particularly those involving the modulation of gut microbiota, remain unexplored. Purpose This study aimed to evaluate the efficacy of Sal B in mitigating acute alcoholic liver injury and rectifying dysbiosis of intestinal microbiota in mice. Materials and Methods Alcohol was used to induce liver injury, and Sal B was used for prevention in mice. Serum biochemical parameters were tested using an automatic hematology analyzer. Pathological alterations in hepatic tissue were assessed using hematoxylin–eosin staining. The mRNA expression levels of specific genes were quantified via reverse transcription polymerase chain reaction, while protein expression was evaluated through Western blot analysis. The composition of the intestinal microbiota in mice was characterized by sequencing the V3–V4 region of the 16S rRNA gene. Results Administration of Sal B resulted in decreased levels of aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, as well as increased levels of total protein and albumin, in mice with acute alcohol-induced liver injury. Furthermore, Sal B effectively reduced hepatic cell degeneration and necrosis, suppressed the expression of toll-like receptor 4, nuclear transcription factor-κB, and phosphorylated nuclear transcription factor-κB proteins in liver tissue. Additionally, Sal B maintained intestinal function in the host. Conclusion Sal B may ameliorate ethanol-induced hepatic injury in mice by modulating the gut microbiota and influencing the TLR4/NF-κB signaling pathway.