title: Dietary fish oil reduces progression of chronic inflammatory lesions in a rat model of granulomatous colitis.
abstract: Eicosanoids are modulators of defensive and inflammatory processes in the gut mucosa, and may be involved in the pathogenesis of chronic inflammatory lesions of the bowel. As omega-3 fatty acids compete with the omega-6 as precursors of eicosanoid synthesis, we compared the effects of dietary supplementation with either sunflower (source of omega-6) or cod liver (source of omega-3) oil on the development of chronic granulomatous lesions in the rat colon. After four weeks on the supplemented diets, plasma omega-6 fatty acid content was significantly higher in the sunflower group, while omega-3 fatty acids predominated in the cod liver group. Inflammatory colitis was then induced by intracolonic administration of trinitrobenzene sulphonic acid. Luminal eicosanoid release, as measured by radioimmunoassay of intracolonic dialysis fluid, increased significantly after the challenge in both groups. Generation of prostaglandin E2 (PGE2) and leucotriene B4 (LTB4) peaked by day 3 and thereafter declined; thromboxane B2 (TXB2), instead, continued to increase from day 3 to 20 in sunflower fed rats, whereas this change was blunted in cod liver animals. The rats were killed 20, 30, or 50 days after the induction of colitis, and the colonic lesions were scored macroscopically (adhesions to surrounding tissues, strictures, ulcerations, and wall thickness) and histologically (ulceration, inflammation, depth of the lesions, and fibrosis). In cod liver animals, the damage score was markedly reduced by day 30, and inflammation and ulceration were almost absent by day 50. In conclusion, a fish oil diet prevents the increase in thromboxane in the chronic state of inflammation and shortens the course of the colonic disease by diminishing both the severity of the lesions and their progression to chronicity.
authors.affiliation: Hospital General Vall d'Hebron, Autonomous University of Barcelona, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Vilaseca
authors.forename: A
authors.initials: A
authors.lastname: Salas
authors.forename: F
authors.initials: F
authors.lastname: Guarner
authors.forename: R
authors.initials: R
authors.lastname: Rodríguez
authors.forename: M
authors.initials: M
authors.lastname: Martínez
authors.forename: J R
authors.initials: JR
authors.lastname: Malagelada
mesh_terms: D000818:Animals; D001835:Body Weight; D003060:Cod Liver Oil / Q000008:administration & dosage*; D003424:Crohn Disease / Q000097:blood / Q000139:chemically induced / Q000517:prevention & control*; D004041:Dietary Fats / Q000627:therapeutic use*; D015232:Dinoprostone / Q000097:blood; D005227:Fatty Acids / Q000097:blood; D015525:Fatty Acids, Omega-3 / Q000097:blood; D005395:Fish Oils / Q000008:administration & dosage*; D006368:Helianthus; D007975:Leukotriene B4 / Q000097:blood; D008297:Male; D010938:Plant Oils / Q000008:administration & dosage; D051381:Rats; D011919:Rats, Inbred Strains; D013929:Thromboxane B2 / Q000097:blood; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D004041:Dietary Fats; D005227:Fatty Acids; D015525:Fatty Acids, Omega-3; D005395:Fish Oils; D010938:Plant Oils; D007975:Leukotriene B4; D013929:Thromboxane B2; D003060:Cod Liver Oil; D014302:Trinitrobenzenesulfonic Acid; D015232:Dinoprostone