Dietary fiber down-regulates colonic tumor necrosis factor alpha and nitric oxide production in trinitrobenzenesulfonic acid-induced colitic rats.
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 alpha (TNFalpha) 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 TNFalpha 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 TNFalpha and NO.
Rodríguez-Cabezas
Maria Elena
ME
Department of Pharmacology, School of Pharmacy, and. Department of Parasitology, School of Sciences, University of Granada, Spain.
Gálvez
Julio
J
Lorente
Maria Dolores
MD
Concha
Angel
A
Camuesco
Desirée
D
Azzouz
Shamira
S
Osuna
Antonio
A
Redondo
Luis
L
Zarzuelo
Antonio
A
D000230:Adenocarcinoma / Q000378:metabolism; D000818:Animals; D020148:Butyric Acid / Q000378:metabolism / Q000494:pharmacology; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism / Q000628:therapy*; D003106:Colon / Q000378:metabolism* / Q000473:pathology; D003110:Colonic Neoplasms / Q000378:metabolism; D004043:Dietary Fiber / Q000627:therapeutic use*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D011422:Propionates / Q000378:metabolism / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014302:Trinitrobenzenesulfonic Acid; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D004043:Dietary Fiber; D016209:Interleukin-8; D011422:Propionates; D014409:Tumor Necrosis Factor-alpha; D020148:Butyric Acid; D009569:Nitric Oxide; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase; D019001:Nitric Oxide Synthase; D005978:Glutathione; C029658:propionic acid