Salvianolic acid B inhibits ERK signal transduction pathway activated by transforming growth factor-β1 in rat hepatic stellate cells

Abstract

To investigate the effects of salvianolic acid B (SA-B) on extracellular signal-regulated kinase (ERK) signal transduction pathway activated by transforming growth factor-β1 (TGF-β1) in rat hepatic stellate cells (HSCs). HSCs were isolated from male Sprague-Dawley rats by in situ perfusion and Nycodenz density-gradient centrifugation method. TGF-β1 and SA-B were directly added to the serum-free medium of HSCs. Total and phosphorylated ERK, MEK, Raf and α-smooth muscle actin (α-SMA) and type I collagen were assayed by Western blotting. Phosphorylation of MEK in HSCs with or without TGF-β1 was inhibited by SA-B; however, phosphorylation of Raf in HSCs with or without TGF-β1 was not inhibited by SA-B. Expression of α-SMA in HSCs with TGF-β1 was inhibited by SA-B. Combination of SA-B and the inhibitors of ERK (PD98059) can effectively inhibit the expression of α-SMA. SA-B also inhibited synthesization of type I collagen in HSCs with or without TGF-β1. The action point of SA-B inhibiting ERK signaling induced by TGF-β1 in HSCs is the inhibition of the phosphorylation of MEK. SA-B reduces the increase of expression of α-SMA and protein synthesization of type I collagen induced by TGF-β1 by means of inhibiting ERK signaling in activated HSCs of rats.