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| Effect of salvianolic acid B on Smad3 expression in hepatic stellate cells |
| Jun-Fang Zhao, Cheng-Hai Liu, Yi-Yang Hu, Lie-Ming Xu, Ping Liu and Cheng Liu |
Shanghai, China
Author Affiliations: Institute of Liver Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai 200023, China (Zhao JF, Liu CH, Hu YY, Xu LM, Liu P and Liu C)
Corresponding Author: Cheng-Hai Liu, MD, Institute of Liver Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai 200023, China (Tel: 86-21-51322443; Fax: 86-21-51322445; Email: chenghailiu@hotmail.com) |
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Abstract 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-β1 (TGF-β1) 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-β1 signaling at HSC.
METHODS: Hepatic stellate cells (HSCs) were isolated, cultured, and incubated with SA-B. The TGF-β1 content in the supernatant of subcultured HSCs was assayed with ELISA. Type I collagen and Smad3 protein in TGF-β1-stimulated primarily cultured HSCs for 4 days were detected by Western blot.
RESULTS: TGF-β1 secreted in activated HSCs was more than in primary HSCs, and SA-B significantly decreased TGF-β1 secretion in activated HSCs. TGF-β1 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-β1 secretion in activated HSCs and counteracts the expression of TGF-β1 stimulated type I collagen and Smad3. These actions are associated with the effect of SA-B on liver fibrosis.
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2004, Vol. 3 
