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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 960128, 11 pages
Research Article

Salvianolic Acid B Inhibits ERK and p38 MAPK Signaling in TGF- 1-Stimulated Human Hepatic Stellate Cell Line (LX-2) via Distinct Pathways

Zhigang Lv1,2,3 and Lieming Xu1,2,4,5

1Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
2Institute of Liver Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
3Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA
4Key Laboratory of Liver and Kidney Diseases, Shanghai University of Traditional Chinese Medicine, Ministry of Education, Shanghai 200444, China
5E-Institute of Traditional Chinese Medicine Internal Medicine in Shanghai University, Shanghai 201203, China

Received 15 December 2010; Revised 13 April 2011; Accepted 22 May 2011

Academic Editor: Xiu-Min Li

Copyright © 2012 Zhigang Lv and Lieming Xu. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Salvianolic acid B (SA-B) is water-soluble component of Radix Salvia miltiorrhiza. The previous work indicated that SA-B can inhibit MAPK and Smad signaling in activated hepatic stellate cells (HSCs) to perform anti-fibrotic activity Lv et al. 2010. However, some studies have shown that there is cross-talk between MAPK and Smad in certain cell types. Thus, the anti-fibrotic action of SA-B may be through the cross-talk. In order to clarify the mechanism of SA-B further, we knocked down Smad in LX-2 cells (SRV4) via RNAi, and then added TGF-β1, and PD98059 or SB203580 and SA-B. The levels of p-MEK and p-p38 were inhibited by SA-B in SRV4 independent of TGF-β1. The expression of Col I and α-SMA in SRV4 could be reduced by SA-B independent TGF-β1. SB203580 had not significant effect on p-MEK in SRV4 stimulated by TGF-β1. The levels of p-MEK in SRV4 were not increased significantly after TGF-β1 stimulation. PD98059 had no effect on the levels of p-p38 in SRV4 irrespective of TGF-β1. In conclusion, SA-B inhibits the synthesis of Col I in LX-2 cells independent of TGF-β1 stimulation, and the anti-fibrotic effect of SA-B is due to direct inhibition of p38 signaling and inhibition the cross-talk of Smad to ERK signaling.