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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 160726, 10 pages
http://dx.doi.org/10.1155/2012/160726
Research Article

Salvianolic Acid B Attenuates Rat Hepatic Fibrosis via Downregulating Angiotensin II Signaling

1Institute of Liver Diseases, ShuGuang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
2Department of Traditional Chinese Medicine, Changhai Hospital, Second Military Medical University, Shanghai 200433, China
3Shanghai Key Laboratory of Traditional Chinese Clinic Medicine, Shanghai 201203, China
4E-Institute of TCM Internal Medicine, Shanghai Municipal Education Commission, Shanghai 201203, China

Received 10 July 2012; Revised 30 September 2012; Accepted 10 October 2012

Academic Editor: Adair Roberto Soares Santos

Copyright © 2012 Shu Li et al. 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.

Abstract

The renin-angiotensin system (RAS) plays an important role in hepatic fibrosis. Salvianolic acid B (Sal B), one of the water-soluble components from Radix Salviae miltiorrhizae, has been used to treat hepatic fibrosis, but it is still not clear whether the effect of Sal B is related to angiotensin II (Ang II) signaling pathway. In the present study, we studied Sal B effect on rat liver fibrosis and Ang-II related signaling mediators in dimethylnitrosamine-(DMN-) induced rat fibrotic model in vivo and Ang-II stimulated hepatic stellate cells (HSCs) in vitro, with perindopril or losartan as control drug, respectively. The results showed that Sal B and perindopril inhibited rat hepatic fibrosis and reduced expression of Ang II receptor type 1 (AT1R) and ERK activation in fibrotic liver. Sal B and losartan also inhibited Ang II-stimulated HSC activation including cell proliferation and expression of type I collagen I (Col-I) and α-smooth muscle actin ( -SMA) production in vitro, reduced the gene expression of transforming growth factor beta (TGF- ), and downregulated AT1R expression and ERK and c-Jun phosphorylation. In conclusion, our results indicate that Sal B may exert an antihepatic fibrosis effect via downregulating Ang II signaling in HSC activation.