A limited role of p53 on the ability of a hexane fraction of American ginseng to suppress mouse colitis

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DOIResolve DOI: http://doi.org/10.1155/2012/785739
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TypeArticle
Journal titleJournal of Biomedicine and Biotechnology
ISSN1110-7243
Volume2012
Article number785739
Subjectginseng extract; protein p53; hexane; plant extract; protein p53; American ginseng; animal experiment; animal model; animal tissue; antiinflammatory activity; apoptosis; article; cell cycle arrest; colon cancer; controlled study; gene mutation; ginseng; human; human cell; in vitro study; in vivo study; mouse; nonhuman; ulcerative colitis; animal; cell line; chemistry; colitis; colon; disease model; drug effect; fractionation; G1 phase cell cycle checkpoint; metabolism; nick end labeling; Panax; pathology; phytotherapy; Animals; Apoptosis; Cell Line; Chemical Fractionation; Colitis; Colon; Disease Models, Animal; G1 Phase Cell Cycle Checkpoints; Hexanes; Humans; In Situ Nick-End Labeling; Mice; Panax; Phytotherapy; Plant Extracts; Tumor Suppressor Protein p53
AbstractUlcerative 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. © Copyright 2012 Deepak Poudyal et al.
Publication date
LanguageEnglish
AffiliationNational Research Council Canada (NRC-CNRC); NRC Institute for National Measurement Standards (INMS-IENM)
Peer reviewedYes
NPARC number21269152
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Record identifier9c0a5aae-a70e-4c21-8cc0-f623c0747909
Record created2013-12-12
Record modified2016-05-09
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