American ginseng suppresses inflammation and DNA damage associated with mouse colitis.
Ulcerative colitis (UC) is a dynamic, idiopathic, chronic inflammatory condition associated with a high colon cancer risk. American ginseng has antioxidant properties and targets many of the players in inflammation. The aim of this study was to test whether American ginseng extract prevents and treats colitis. Colitis in mice was induced by the presence of 1% dextran sulfate sodium (DSS) in the drinking water or by 1% oxazolone rectally. American ginseng extract was mixed in the chow at levels consistent with that currently consumed by humans as a supplement (75 p.p.m., equivalent to 58 mg daily). To test prevention of colitis, American ginseng extract was given prior to colitis induction. To test treatment of colitis, American ginseng extract was given after the onset of colitis. In vitro studies were performed to examine mechanisms. Results indicate that American ginseng extract not only prevents but it also treats colitis. Inducible nitric oxide synthase and cyclooxygenase-2 (markers of inflammation) and p53 (induced by inflammatory stress) are also downregulated by American ginseng. Mucosal and DNA damage associated with colitis is at least in part a result of an oxidative burst from overactive leukocytes. We therefore tested the hypothesis that American ginseng extract can inhibit leukocyte activation and subsequent epithelial cell DNA damage in vitro and in vivo. Results are consistent with this hypothesis. The use of American ginseng extract represents a novel therapeutic approach for the prevention and treatment of UC.
Jin
Yu
Y
Department of Pharmaceutical and Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina, SC 29208, USA.
Kotakadi
Venkata S
VS
Ying
Lei
L
Hofseth
Anne B
AB
Cui
Xiangli
X
Wood
Patricia A
PA
Windust
Anthony
A
Matesic
Lydia E
LE
Pena
Edsel A
EA
Chiuzan
Codruta
C
Singh
Narendra P
NP
Nagarkatti
Mitzi
M
Nagarkatti
Prakash S
PS
Wargovich
Michael J
MJ
Hofseth
Lorne J
LJ
D000818:Animals; D015153:Blotting, Western; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy*; D020552:Comet Assay; D051546:Cyclooxygenase 2 / Q000187:drug effects; D004249:DNA Damage / Q000187:drug effects*; D016264:Dextran Sulfate / Q000633:toxicity; D005455:Fluorescent Antibody Technique; D019073:HT29 Cells; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000188:drug therapy*; D008262:Macrophage Activation / Q000187:drug effects; D008264:Macrophages / Q000187:drug effects; D051379:Mice; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects; D005894:Panax; D008517:Phytotherapy / Q000379:methods; D010936:Plant Extracts / Q000627:therapeutic use*; D016897:Respiratory Burst / Q000187:drug effects; D016159:Tumor Suppressor Protein p53 / Q000187:drug effects
D010936:Plant Extracts; D016159:Tumor Suppressor Protein p53; D016264:Dextran Sulfate; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2
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