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Evidence-Based Complementary and Alternative Medicine
Volume 2015 (2015), Article ID 645727, 12 pages
http://dx.doi.org/10.1155/2015/645727
Research Article

Plumbagin Ameliorates CCl4-Induced Hepatic Fibrosis in Rats via the Epidermal Growth Factor Receptor Signaling Pathway

1Department of Hepatopathy, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, China
2Wenzhou Key Laboratory of Hepatology, Department of Infectious Disease, Hepatology Institute of Wenzhou Medical University, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China
3Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China
4Department of Urology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China
5Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong

Received 10 July 2015; Revised 25 August 2015; Accepted 26 August 2015

Academic Editor: Yuewen Gong

Copyright © 2015 Si Chen 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

Epidermal growth factor (EGF) and its signaling molecules, EGFreceptor (EGFR) and signal transducer and activator of transcription factor 3 (STAT3), have been considered to play a role in liver fibrosis and cirrhosis. Plumbagin (PL) is an extracted component from the plant and has been used to treat different kinds of cancer. However, its role in regulation of EGFR and STAT3 during liver fibrosis has not been investigated. In this study, the effects of PL on the regulation of EGFR and STAT3 were investigated in carbon tetrachloride (CCl4) induced liver fibrosis and hepatic stellate cells (HSC-T6). PL significantly attenuated liver injury and fibrosis in CCl4 treated rats. At concentrations of 2 to 6 μM, PL did not induce significant cytotoxicity of HSC-T6 cells. Moreover, PL reduced phosphorylation of EGFR and STAT3 in both fibrotic liver and heparin-binding EGF-like growth factor (HB-EGF) treated HSC-T6 cells. Furthermore, PL reduced the expression of α-SMA, EGFR, and STAT3 in both fibrotic liver and HB-EGF treated HSC-T6 cells. In conclusion, plumbagin could ameliorate the development of hepatic fibrosis through its downregulation of EGFR and STAT3 in the liver, especially in hepatic stellate cells.