Volume 26, Issue 8 pp. 1298-1308

Prebiotic treatment in experimental colitis reduces the risk of colitic cancer

Yutaka Komiyama

Yutaka Komiyama

Central Laboratories for Frontier Technology, Kirin Holdings Co. Ltd., Yokohama, Japan

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Keiichi Mitsuyama

Keiichi Mitsuyama

Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan

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Jyunya Masuda

Jyunya Masuda

Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan

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Hiroshi Yamasaki

Hiroshi Yamasaki

Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan

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Hidetoshi Takedatsu

Hidetoshi Takedatsu

Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan

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Akira Andoh

Akira Andoh

Division of Mucosal Immunology, Graduate School of Medicine, Shiga University of Medical Science, Shiga, Japan

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Osamu Tsuruta

Osamu Tsuruta

Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan

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Masanobu Fukuda

Masanobu Fukuda

Department of Clinical Pharmacokinetics, College of Pharmacy, Nihon University, Funabashi, Japan

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Osamu Kanauchi

Corresponding Author

Osamu Kanauchi

Central Laboratories for Frontier Technology, Kirin Holdings Co. Ltd., Yokohama, Japan

Dr Osamu Kanauchi, Central Laboratories for Frontier Technology, Kirin Holdings Co. Ltd., 1-13-5, Fukuura Kanzawa-ku, Yokohama 236-0004, Japan. Email: [email protected]Search for more papers by this author
First published: 09 February 2011
Citations: 18

Abstract

Background and Aim: Germinated barley foodstuff (GBF) is a prebiotic product that reduces colonic mucosal inflammation and the clinical symptoms observed in ulcerative colitis (UC). The risk of contracting colorectal cancer is higher in patients with UC than in that of the general population. The aim of this study is to apply this prebiotic approach to control chronic colitis and to reduce the incidence of colitic cancer.

Methods: Repeated and intermitted dextran sulfate sodium administration to male Sprague–Dawley rats was used for the chronic and subacute colitis models. GBF was added as the diet (10% w/v). The incidence of adenomatous high-grade dysplasia, and pathophysiological observations, including the proliferative cell nuclear antigen (PCNA) labeling index, and clinical score, cecal organic acid profile, and the accompanying β-glucosidase activity were determined.

Results: In the chronic phase, the incidence of adenomatous dysplasia was only confirmed in the control group, and the GBF group had no dysplasia in the entire colon; the stratified squamous epithelium area of GBF was significantly lower than that of the controls. GBF treatment significantly lowered the cecal succinate content and significantly increased β-glucosidase activity compared to the controls. In addition, colonic mucosal inflammatory damage was comparable between the two groups, while the PCNA labeling index of the colonic mucosa in the GBF group was significantly lower than that of the control group. However, in the subacute phase, the mucosal damage score of GBF was significantly attenuated, and the PCNA labeling index of the colonic mucosa in the GBF group was significantly higher than that of the control group.

Conclusion: This preliminary study demonstrated that GBF effectively prevents colitis-related dysplasia and inflammatory change in chronic and subacute colitis models by modulating the intestinal environment as a prebiotic. This prebiotic might contribute to the prevention of mucosal damage, to show different proliferative effects on the epithelium in the regeneration and steady states.

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