Germinated Barley Foodstuffs Attenuate Colonic Mucosal Damage and Mucosal Nuclear Factor Kappa B Activity in a Spontaneous Colitis
Germinated barley foodstuffs attenuate colonic mucosal damage and mucosal nuclear factor kappa B activity in a spontaneous colitis model
J Gastroenterol Hepatol. 1999 Dec;14(12):1173-9
Kanauchi O, Andoh A, Iwanaga T, Fujiyama Y, Mitsuyama K, Toyonaga A, Bamba T.
Applied Bioresearch Center, Corporate Research and Development Division, Kirin Brewery Co. Ltd, Gunma, Japan.
BACKGROUND: Germinated barley foodstuffs (GBF), which are derived from brewer’s spent grain and are a highly safe food substance, increased butyrate production in the lower intestine and prevented mucosal damage and bloody diarrhoea in an acute experimental colitis model. As human histocompatibility leucocyte antigen (HLA)-B27 transgenic rats develop spontaneous and chronic intestinal inflammation resembling ulcerative colitis, we investigated the mechanisms underlying the preventive effects of GBF against a spontaneous and chronic colitis model. Specifically, the production of bacterial butyrate and the regulation of proinflammatory cytokine production were examined.
METHODS: A GBF diet and a cellulose (CE) diet were fed to HLA-B27 transgenic rats for 13 weeks. The presence of faecal occult blood, colonic mucosal protein, DNA and RNA content, colonic myeloperoxidase activity, nuclear factor kappa B (NFkappaB) DNA binding activity, the depth of the crypts and serum inflammatory parameters were then evaluated. Butyrate production in the caecal contents was also determined.
RESULTS: Feeding GBF significantly increased bacterial butyrate production and simultaneously attenuated the presence of faecal occult blood and colonic mucosal hyperplasia. Colonic mucosal NFkappaB-DNA binding activity and the production of interleukin-8 were also suppressed by the butyrate produced from GBF.
CONCLUSIONS: Germinated barley foodstuffs feeding promotes bacterial butyrate production and attenuated inflammation in both spontaneous and chronic colitis in HLA-B27 transgenic rats.