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Evidence-Based Complementary and Alternative Medicine
Volume 2015 (2015), Article ID 194373, 8 pages
Research Article

Sedum mexicanum Britt. Induces Apoptosis of Primary Rat Activated Hepatic Stellate Cells

1Department of Biological Science and Technology, College of Life Sciences, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan
2Department of Bioscience Technology, Chung Yuan Christian University, 200 Chung Pei Road, Taoyuan 32023, Taiwan
3Department of Nursing, Chang Gung University of Science and Technology, 261 Wenhwa 1st Road, Taoyuan 33303, Taiwan
4Department of Biotechnology, Asia University, 500 Lioufeng Road, Taichung 41354, Taiwan

Received 19 January 2015; Revised 28 April 2015; Accepted 4 May 2015

Academic Editor: Yibin Feng

Copyright © 2015 Shou-Lun Lee 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.


Background. Liver fibrosis is a significant liver disease in Asian countries. Sedum mexicanum Britt. (SM) has been claimed to have antihepatitis efficacy. In traditional folk medicine, a solution of boiling water-extracted SM (SME) is consumed to prevent and treat hepatitis. However, its efficacy has not yet been verified. The purpose of this study was to investigate the in vitro effect of SME on hepatoprotection. Methods. Hepatic stellate cells (HSCs) and hepatocytes (HCs) were isolated from the livers of the rats by enzymatic digestion and density gradient centrifugation. Results. Treating the HCs and aHSCs with SME caused a dose-dependent decrease in the viability of aHSCs but not that of HCs. In addition, treatment with SME resulted in apoptosis of aHSCs, as determined by DAPI analysis and flow cytometry. SME also increased the amount of cleaved caspase-3, cleaved caspase-9, and cleaved poly ADP-ribose polymerase (PARP) in aHSCs. Furthermore, SME treatment induced a dose-dependent reduction in Bcl-2 expression and increased the expression of Bax in aHSCs. Conclusions. SME did not cause cytotoxicity in HCs, but it induced apoptosis in aHSCs through the mitochondria-dependent caspase-3 pathway. Therefore, SME may possess therapeutic potential for liver fibrosis.