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Biochemical and Molecular Actions of Nutrients

Dietary Fiber Down-Regulates Colonic Tumor Necrosis Factor and Nitric Oxide Production in Trinitrobenzenesulfonic Acid-Induced Colitic Rats^{1 ,2}

Maria Elena Rodríguez-Cabezas^*, Julio Gálvez^*,34, Maria Dolores Lorente^*, Angel Concha^**, Desirée Camuesco^*, Shamira Azzouz, Antonio Osuna, Luis Redondo and Antonio Zarzuelo^*,3

^* Department of Pharmacology, School of Pharmacy, and Department of Parasitology, School of Sciences, University of Granada, Spain, ^** Department of Pathology, Hospital Universitario "Virgen de las Nieves," Granada, Spain and Madaus Laboratories S.A., Barcelona, Spain

⁴To whom correspondence should be addressed. E-mail: jgalvez{at}ugr.es.

Previous studies have revealed the beneficial effects exerted by dietary fiber in human inflammatory bowel disease, which were associated with an increased production of SCFA in distal colon. The aim of the present study was to elucidate the probable mechanisms involved in the beneficial effects of a fiber-supplemented diet (5% Plantago ovata seeds) in the trinitrobenzenesulfonic acid (TNBS) model of rat colitis, with special attention to its effects on the production of some of the mediators involved in the inflammatory response, such as tumor necrosis factor (TNF) and nitric oxide (NO). Rats were fed the fiber-supplemented diet for 2 wk before TNBS colitis induction and thereafter until colonic evaluation 1 wk later. The results obtained showed that dietary fiber supplementation facilitated recovery from intestinal insult as evidenced both histologically, by a preservation of intestinal cytoarchitecture, and biochemically, by a significant reduction in colonic myeloperoxidase activity and by restoration of colonic glutathione levels. This intestinal anti-inflammatory effect was associated with lower TNF levels and lower NO synthase activity in the inflamed colon, showing significant differences when compared with nontreated colitic rats. Moreover, the intestinal contents from fiber-treated colitic rats showed a significantly higher production of SCFA, mainly butyrate and propionate. We conclude that the increased production of these SCFA may contribute to recovery of damaged colonic mucosa because they constitute substrates for the colonocyte and, additionally, that they can inhibit the production of proinflammatory mediators, such as TNF and NO.

KEY WORDS: • dietary fiber • rat colitis • tumor necrosis factor • nitric oxide synthase • short chain fatty acids

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