title: An α-linolenic acid-rich formula reduces oxidative stress and inflammation by regulating NF-κB in rats with TNBS-induced colitis.
abstract: We have previously shown that α-linolenic acid (ALA), a (n-3) PUFA exerts in vitro antiinflammatory effects in the intestine. In this study, we aimed to evaluate its effect on inflammatory and oxidative stress in a colitis model. Colitis was induced in 2 groups at d 0 by intrarectal injection of 2-4-6-trinitrobenzen sulfonic acid (TNBS), whereas the control group received the vehicle. Rats we fed 450 mg . kg(-1) . d(-1) of ALA (TNBS+ALA) while the other colitic group (TNBS) and the control group were fed an isocaloric corn oil formula for 14 d (from d -7 to d 7). RBC fatty acid composition was assessed. Oxidative stress was studied by measuring urinary 8-isoprostanes (8-IP) and colon glutathione (GSH) concentration and inducible nitric oxide synthase (iNOS) expression. Colitis was assessed histologically, by production of proinflammatory mediators, including cytokines, leukotrienes B(4) (LTB(4)), and cyclooxygenase-2 (COX-2) and by nuclear factor-κB (NF-κB) activation. The ALA-rich diet significantly increased the RBC levels of ALA, eicosapentaenoic acid, and docosapentaenoic acid (n-3) compared with the TNBS group (P < 0.01 for all). The beneficial effect of ALA supplementation on oxidative stress was reflected by lower urinary 8-IP levels (P < 0.05), a normalized colon GSH concentration (P < 0.01), and reduced colon iNOS expression (P < 0.05) compared with the TNBS group. ALA also protected against colon inflammation as assessed by lower tumor necrosis factor-α secretion and mRNA level (P < 0.05), reduced NF-κB activation (P = 0.01), and lower colon lipid mediator concentrations such as LTB(4) and COX-2 (P < 0.05) compared with the TNBS group. These findings show that an ALA-rich formula is beneficial to TNBS-induced colitic rats via inhibition of oxidative and inflammatory stress.
authors: Appareil Digestif Environnement Nutrition, Medicine University, I.F.R. 23, Institute of biomedical research, 22, 76183 Rouen cedex, France.
authors: Aktham
authors: A
authors: Hassan
authors: Ayman
authors: A
authors: Ibrahim
authors: Khaly
authors: K
authors: Mbodji
authors: Moïse
authors: M
authors: Coëffier
authors: Frédéric
authors: F
authors: Ziegler
authors: Frédéric
authors: F
authors: Bounoure
authors: Jean-Michel
authors: JM
authors: Chardigny
authors: Mohamed
authors: M
authors: Skiba
authors: Guillaume
authors: G
authors: Savoye
authors: Pierre
authors: P
authors: Déchelotte
authors: Rachel
authors: R
authors: Marion-Letellier
mesh_terms: D000818:Animals; D002918:Chymotrypsin / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism* / Q000517:prevention & control*; D003106:Colon / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000032:analysis; D004032:Diet; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D015777:Eicosanoids / Q000096:biosynthesis; D004912:Erythrocytes / Q000737:chemistry; D005227:Fatty Acids / Q000097:blood; D005978:Glutathione / Q000032:analysis; D007372:Interferons / Q000032:analysis; D008297:Male; D016328:NF-kappa B / Q000032:analysis / Q000187:drug effects* / Q000502:physiology; D052247:Nitric Oxide Synthase Type II / Q000032:analysis; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014302:Trinitrobenzenesulfonic Acid / Q000008:administration & dosage; D017962:alpha-Linolenic Acid / Q000008:administration & dosage*
chemical_list: D016207:Cytokines; D015777:Eicosanoids; D005227:Fatty Acids; D016328:NF-kappa B; D017962:alpha-Linolenic Acid; C075750:8-epi-prostaglandin F2alpha; D014302:Trinitrobenzenesulfonic Acid; D007372:Interferons; D015237:Dinoprost; D052247:Nitric Oxide Synthase Type II; D002918:Chymotrypsin; D005978:Glutathione