The fundamental feature of liver fibrosis is the abnormal activation of HSCs, and BBR has been shown to be a potential treatment for thioacetamide (TAA)-, CCl4-, ethanol- and high cholesterol-induced liver fibrosis models; in these contexts, it likely acts by suppressing HSC activation and downregulating alpha-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) levels. This evidence concerns the gene ACTA1 and Hepatic fibrosis.