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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 682418, 12 pages
Research Article

Inhibition of Helicobacter pylori CagA-Induced Pathogenesis by Methylantcinate B from Antrodia camphorata

1Graduate Institute of Clinical Medical Science, China Medical University, Taichung 40402, Taiwan
2Institute of Biochemical Sciences and Technology, Chaoyang University of Technology, Taichung 41349, Taiwan
3Department of Biochemistry and Molecular Medicine, University of California Davis Comprehensive Cancer Center, Sacramento, CA 95817, USA
4Department of Internal Medicine, China Medical University Hospital, Taichung 40402, Taiwan
5Institute of Genomics and Bioinformatics, National Chung Hsing University, Taichung 40227, Taiwan
6Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan
7Department of Microbiology and Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan

Received 11 October 2012; Accepted 23 December 2012

Academic Editor: Mohd Roslan Sulaiman

Copyright © 2013 Chun-Jung Lin 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.


The bacterial pathogen Helicobacter pylori (Hp) is the leading risk factor for the development of gastric cancer. Hp virulence factor, cytotoxin-associated gene A (CagA) interacted with cholesterol-enriched microdomains and leads to induction of inflammation in gastric epithelial cells (AGS). In this study, we identified a triterpenoid methylantcinate B (MAB) from the medicinal mushroom Antrodia camphoratawhich inhibited the translocation and phosphorylation of CagA and caused a reduction in hummingbird phenotype in HP-infected AGS cells. Additionally, MAB suppressed the Hp-induced inflammatory response by attenuation of NF-κB activation, translocation of p65 NF-κB, and phosphorylation of IκB-α, indicating that MAB modulates CagA-mediated signaling pathway. Additionally, MAB also suppressed the IL-8 luciferase activity and its secretion in HP-infected AGS cells. On the other hand, molecular structure simulations revealed that MAB interacts with CagA similarly to that of cholesterol. Moreover, binding of cholesterol to the immobilized CagA was inhibited by increased levels of MAB. Our results demonstrate that MAB is the first natural triterpenoid which competes with cholesterol bound to CagA leading to attenuation of Hp-induced pathogenesis of epithelial cells. Thus, this study indicates that MAB may have a scope to develop as a therapeutic candidate against Hp CagA-induced inflammation.