Abstract:

Objective To investigate the mechanism of salvianolic acid B(SA-B) against liver fibrosis related to TGF-β/ERK signal transduction. Methods NIH/3T3 fibroblasts were divided into 4 groups: normal, model and treated groups with lower and high dosage of SA-B. Except of the normal group, the cells were incubated with 100 pmol/L TGF-β1 for 24 h, and the treated group in-cubated with 1 μmol/L or 10 μmol/L SA-B in 0.5% FBS/M199 at the same time respectively. The NIH/3T3 fibroblast viability was observed with MTT assay. The collagen type I and plasminogen activator inhibitor-1(PAI-1) proteins were analyzed with Western blot. The proteins of TGF-β receptor type Ⅰ and Ⅱ (TβR-Ⅰ, TβR-Ⅱ), ERK1 and its phosphorylation(P44 and P42) were analyzed with Western blot. Results TGF-β1 increased the expression of collagen type Ⅰ protein, improved its PAI-1 production, both of TβR-Ⅰ and Ⅱ protein expression and ERK phosphorylation. MTT assay showed SA-B had no effect on the viability of NIH/3T3 fibroblasts, While SA-B inhibited TGF-β1 stimulated collagen and PAI-1 production in dose-dependent manner, decreased TβR-Ⅰ protein expression, and inhibited ERK phosphorylation, and 10 μmol/L SA-B had a much better effects than 1 μmol/L SA-B. Conclusion SA-B antagonizes the profibrogenic effects of TGF-β1 by inhibiting TβR-Ⅰ expression and ERK phosphorylation, and these actions are associated with the mechanism of SA-B effect against liver fibrosis.

Key words: salvianolic acid B, transforming growth factor-&beta, receptor, extracelluar-signal regulated protein kinase(ERK), liver fibrosis