Table of Contents Author Guidelines Submit a Manuscript
Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 785739, 11 pages
Research Article

A Limited Role of p53 on the Ability of a Hexane Fraction of American Ginseng to Suppress Mouse Colitis

1Department of Pharmaceutical and Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina and Medical University of South Carolina, Columbia, SC 29208, USA
2Institute for National Measurement Standards, National Research Council, Ottawa, ON, Canada K1A 0R6
3Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA
4Department of Cell and Molecular Pharmacology & Experimental Therapeutics and Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29245, USA
5School of Medicine, University of South Carolina, Columbia, SC 29208, USA

Received 22 March 2012; Revised 25 May 2012; Accepted 11 June 2012

Academic Editor: Paul W. Doetsch

Copyright © 2012 Deepak Poudyal 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.


Ulcerative colitis (UC) is debilitating and carries a high colon cancer risk. Apoptosis of inflammatory cells is a key mechanism regulating UC. We have recently shown that American ginseng (AG), and to a greater extent, a Hexane fraction of AG (HAG) can cause apoptosis and suppress mouse colitis through a p53-mediated mechanism. Here, we tested the hypothesis that HAG suppresses colitis through a p53 mechanism. We found only a limited impact of p53 in the ability of HAG to induce inflammatory cell apoptosis and suppress mouse colitis in vitro and in vivo. Finally, we asked whether HAG could cause cell cycle arrest of HCT116 colon cancer cells in vitro. Interestingly, HAG caused a G1 arrest of such cells independent of p53 status. Findings are significant because HAG suppresses colitis and associated colon cancer, and mutation in p53 is observed in most colitis-driven colon cancers. Therefore, HAG might be very effective in targeting the inflammatory cells and cancer cells since it induces apoptosis of inflammatory cells and cell cycle arrest in both p53−/− and WT p53 colon cancer cells.