Inhibition by Ginseng of Colon Carcinogenesis in Rats.
10.3346/jkms.2001.16.S.S75
- Author:
Shoji FUKUSHIMA
1
;
Hideki WANIBUCHI
;
Wei LI
Author Information
1. Department of Pathology, Osaka City University Medical School, Osaka, Japan. fukuchan@med.osaka-cu.ac.jp
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Ginseng;
1,2-Dimethylhydrazine;
Rat Colon Carcinogenesis;
Aberrant Crypt Foci
- MeSH:
1,2-Dimethylhydrazine/adverse effects;
Animal;
Anticarcinogenic Agents/*pharmacology;
Carcinogenicity Tests;
Carcinogens/adverse effects;
Colonic Neoplasms/pathology/*prevention & control;
Male;
*Panax;
Plant Roots;
Precancerous Conditions/pathology/*prevention & control;
Rats;
Rats, Inbred F344
- From:Journal of Korean Medical Science
2001;16(Suppl):S75-S80
- CountryRepublic of Korea
- Language:English
-
Abstract:
The inhibitory effects of ginseng on the development of 1,2-dimethylhydrazine (DMH)-induced aberrant crypt foci (ACF) in the colon were investigated in rats. Male, 6-week-old rats were injected with DMH once a week for 4 weeks. Rats in Groups 1 and 2 were fed diets containing red and white ginseng, rerspectively, at a dose of 1% for 5 weeks, starting one week before the first treatment of DMH. Animals in Groups 3 and 4 received red or white ginseng for 8 weeks starting after DMH treatment. Group 5 served as a carcinogen control group. Numbers of ACF with at least four crypts were significantly reduced in the colon of Group 2 treated with red ginseng combined with DMH. Moreover, rats were injected with DMH 4 times at one-week intervals. They were also fed diets containing 1% red or white ginseng or the control diet throughout 30 days of the experiment. Treatment with red ginseng resulted in a significant decrease of 5- bromo-2'-deoxyuridine labeling indices in colonic crypts comprising ACF. These findings suggest that dietary administration of red ginseng in combination with DMH suppresses colon carcinogenesis in rats, and the inhibition may be associated, in part, with inhibition of cell proliferation, acting on ACF in the colonic mucosa.
