Background: Salvianolic acid B (SA-B), one of water soluble compounds derived from Radix salviae miltiorrhizae, had good action against liver fibrosis of patients with chronic hepatitis. Hepatic stellate cells (HSCs) is the cellular resource for liver fibrogenesis, while transforming growth factor-beta1 (TGF-beta1) is most potent fibrogenic factor. In this study we investigated the mechanism of SA-B action against liver fibrosis relating to the interference with TGF-beta1 signaling at HSC.
Methods: Hepatic stellate cells (HSCs) were isolated, cultured, and incubated with SA-B. The TGF-beta1 content in the supernatant of subcultured HSCs was assayed with ELISA. Type I collagen and Smad3 protein in TGF-beta1-stimulated primarily cultured HSCs for 4 days were detected by Western blot.
Results: TGF-beta1 secreted in activated HSCs was more than in primary HSCs, and SA-B significantly decreased TGF-beta1 secretion in activated HSCs. TGF-beta1 increased the expression of type I collagen and Smad3 protein in d4 primary HSCs, while SA-B inhibited their expression.
Conclusions: SA-B inhibits TGF-beta1 secretion in activated HSCs and counteracts the expression of TGF-beta1 stimulated type I collagen and Smad3. These actions are associated with the effect of SA-B on liver fibrosis.