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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 296082, 17 pages
Research Article

Antcin C from Antrodia cinnamomea Protects Liver Cells Against Free Radical-Induced Oxidative Stress and Apoptosis In Vitro and In Vivo through Nrf2-Dependent Mechanism

1Department of Forestry, National Chung Hsing University, Taichung 402, Taiwan
2Department of Cosmeceutics, China Medical University, Taichung 40402, Taiwan
3Graduate Institute of Veterinary Pathology, National Chung Hsing University, Taichung 402, Taiwan
4The Experimental Forest Management Office, National Chung-Hsing University, Taichung 402, Taiwan
5Department of Food Science and Biotechnology, National Chung Hsing University, Taichung 402, Taiwan
6Taiwan Leader Biotech Company, Taipei 24747, Taiwan
7Graduate Institute of Chinese Pharmaceutical Science, China Medical University, Taichung 40402, Taiwan
8Department of Biotechnology, Asia University, Taichung 41354, Taiwan
9Agricultural Biotechnology Research Center, Academia Sinica, Taipei 115, Taiwan

Received 14 June 2013; Accepted 6 October 2013

Academic Editor: Yew-Min Tzeng

Copyright © 2013 M. Gokila Vani 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.


In this study, we investigated the cytoprotective effects of antcin C, a steroid-like compound isolated from Antrodia cinnamaomea against AAPH-induced oxidative stress and apoptosis in human hepatic HepG2 cells. Pretreatment with antcin C significantly protects hepatic cells from AAPH-induced cell death through the inhibition of ROS generation. Furthermore, AAPH-induced lipid peroxidation, ALT/AST secretion and GSH depletion was significantly inhibited by antcin C. The antioxidant potential of antcin C was correlated with induction of antioxidant genes including, HO-1, NQO-1, γ-GCLC, and SOD via transcriptional activation of Nrf2. The Nrf2 activation by antcin C is mediated by JNK1/2 and PI3K activation, whereas pharmacologic inhibition of JNK1/2 and PI3K abolished antcin C-induced Nrf2 activity. In addition, AAPH-induced apoptosis was significantly inhibited by antcin C through the down-regulation of pro-apoptotic factors including, Bax, cytochrome c, capase 9, -4, -12, -3, and PARP. In vivo studies also show that antcin C significantly protected mice liver from AAPH-induced hepatic injury as evidenced by reduction in hepatic enzymes in circulation. Further, immunocytochemistry analyses showed that antcin C significantly increased HO-1 and Nrf2 expression in mice liver tissues. These results strongly suggest that antcin C could protect liver cells from oxidative stress and cell death via Nrf2/ARE activation.