Inhibition by Ginseng of Colon Carcinogenesis in Rats

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.

Wound healing and colon carcinogenesis: enhancing effects of skin wounding on development of colon tumors induced by 1, 2 Dimethylhydrazine in the rat

This study demonstrates the tumor promoting effect at a distant site of skin wounding, in a model of colon carcinogenesis induced by 1,2 dimethylhydrazine (DMH) in the rat. Six-week-old male Wistar rats were given subcutaneous injections of DMH, 20mg/kg, or saline, once a week, for eight weeks. One week after the last DMH injection the animals received a full thickness skin wound in their dorsal skin and the wound was left open to heal by second intention. Control and DMH-treated rats, with or without skin wounds were killed at the 12th week, just after healing of the skin wound was complete. The colons were removed and divided into proximal and distal parts. Each segment was rolled as "Swiss roll"and processed for histology. The incidence, distribution and morphology of the colon tumors was recorded. The total number of tumors in the colonic mucosa and the number of tumors per rat was significantly higher in the skin-wounding DMH- treated group than in the unwounded group. In the histopathological analysis of the colon the number of poorly differentiated mucin-secreting carcinomas was 6-fold in the skin-wounding DMH-treated group than in the unwounded group and the majority of tumors were located near to lymphoid aggregates. The present results suggest that wound healing enhances tumor development at a distant site, such as the colon, and this effect seems to be related to tumor histology.