MicroRNA-122 mediates the protective effect of baicalin on liver fibrosis

As the most abundant miRNA in the liver, miR-122 has been suggested to be involved in multiple hepatic disorders such as hepatic carcinoma, HCV infection, and non-alcoholic fatty liver disease. However, its role in liver fibrosis is not fully understood. In this study, we tested the potential involvement of miR-122 in liver fibrosis and baicalin-induced improvement of fibrotic changes. Twenty liver fibrosis patients and twenty matched healthy volunteers were enrolled in this study. Serum ALT, AST, and miRNA levels were detected. Liver fibrosis animal model was induced by intraperitoneal injection of CCl4. Patients with liver fibrosis had a reduced serum level of miR-122, accompanied with elevated serum ALT and AST levels. Baicalin dose-dependently modulated CCl4-induced liver damage and collagen deposition, and increased miR-122 expression in both liver and serum. In consistency, KLF6, a direct target of miR-122 which contributes to fibrogenesis, reduced in baicalin-treated mice with hepatic fibrosis. Our study suggests the therapeutic effect of baicalin on hepatic fibrosis may involve miR-122 and its target gene KLF6.