In summary, we found that DBT inhibits angiogenesis in CCl4-induced liver fibrosis in rats in the current study, which is closely related to DBT anti-fibrotic property; and that DBT reduces the expression of HIF-1α, VEGF, TGF-β1, and Ang1, decreases the receptors expression of VEGF-R2, TGFβ-R1/2 and Tie2, downregulates ERK phosphorylation, and improves hepatic oxidative injury in fibrotic liver; these effects contribute to the overall action mechanisms of DBT against liver angiogenesis and fibrosis. Here, TGFB1 is linked to Hepatic fibrosis.