Scandinavian journal of gastroenterology · 2006
A traditional Japanese medicine mitigates TNBS-induced colitis in rats.
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Fukuda Yoshihiro, Tao Yang, Tomita Toshihiko, Hori Kazutoshi, Fukunaga Ken, Noguchi Takayasu, Hayashi Tomoko, Shimoyama Tadashi, Tahahashi Ryoki
Аннотация
OBJECTIVE: Differences in dietary habits may be one of the reasons that the incidence of inflammatory bowel disease has remained lower in Japan than in Western countries. We investigated whether a traditional Japanese medicine (Strong Wakamto), based on Aspergillus oryzae koji, would exert any effect on experimental colitis in rats.
MATERIAL AND METHODS: Colitis was induced using an enema of trinitrobenzene sulfonic acid (TNBS) and ethanol. Strong Wakamto was administered for 28 days before induction of colitis and for 7 days thereafter, and the effect of this medicine was evaluated.
RESULTS: Treatment with 5% Strong Wakamto improved loss of body-weight, increased colon weight and significantly decreased the histological damage score for colon mucosa. Decreases in faecal Lactobacillus sp., superoxide dismutase activity and zinc concentrations, and the increased IL-1beta expression in colonic tissue after TNBS enema were improved when Strong Wakamto was given. The present in vitro studies indicate that administration of Strong Wakamto prevents lipopolysaccharide-induced TNF-alpha production in human macrophages.
CONCLUSIONS: Oral administration of Strong Wakamto mitigates experimental inflammatory bowel disease induced by TNBS enema in rats. The beneficial effects seem attributable to a combination of balancing microflora, immunomodulatory effects on gut macrophages, and enhancement of anti-superoxide activity in colonic tissues.
MATERIAL AND METHODS: Colitis was induced using an enema of trinitrobenzene sulfonic acid (TNBS) and ethanol. Strong Wakamto was administered for 28 days before induction of colitis and for 7 days thereafter, and the effect of this medicine was evaluated.
RESULTS: Treatment with 5% Strong Wakamto improved loss of body-weight, increased colon weight and significantly decreased the histological damage score for colon mucosa. Decreases in faecal Lactobacillus sp., superoxide dismutase activity and zinc concentrations, and the increased IL-1beta expression in colonic tissue after TNBS enema were improved when Strong Wakamto was given. The present in vitro studies indicate that administration of Strong Wakamto prevents lipopolysaccharide-induced TNF-alpha production in human macrophages.
CONCLUSIONS: Oral administration of Strong Wakamto mitigates experimental inflammatory bowel disease induced by TNBS enema in rats. The beneficial effects seem attributable to a combination of balancing microflora, immunomodulatory effects on gut macrophages, and enhancement of anti-superoxide activity in colonic tissues.