Document Detail


An α-linolenic acid-rich formula reduces oxidative stress and inflammation by regulating NF-κB in rats with TNBS-induced colitis.
MedLine Citation:
PMID:  20724486     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Aktham Hassan; Ayman Ibrahim; Khaly Mbodji; Moïse Coëffier; Frédéric Ziegler; Frédéric Bounoure; Jean-Michel Chardigny; Mohamed Skiba; Guillaume Savoye; Pierre Déchelotte; Rachel Marion-Letellier
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Publication Detail:
Type:  Journal Article     Date:  2010-08-19
Journal Detail:
Title:  The Journal of nutrition     Volume:  140     ISSN:  1541-6100     ISO Abbreviation:  J. Nutr.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-21     Completed Date:  2010-10-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0404243     Medline TA:  J Nutr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1714-21     Citation Subset:  IM    
Affiliation:
Appareil Digestif Environnement Nutrition, Medicine University, I.F.R. 23, Institute of biomedical research, 22, 76183 Rouen cedex, France.
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MeSH Terms
Descriptor/Qualifier:
Animals
Chymotrypsin / metabolism
Colitis / chemically induced,  metabolism*,  prevention & control*
Colon / chemistry,  metabolism,  pathology
Cytokines / analysis
Diet
Dinoprost / analogs & derivatives,  urine
Eicosanoids / biosynthesis
Erythrocytes / chemistry
Fatty Acids / blood
Glutathione / analysis
Interferons / analysis
Male
NF-kappa B / analysis,  drug effects*,  physiology
Nitric Oxide Synthase Type II / analysis
Oxidative Stress / drug effects*
Rats
Rats, Sprague-Dawley
Trinitrobenzenesulfonic Acid* / administration & dosage
alpha-Linolenic Acid / administration & dosage*
Chemical
Reg. No./Substance:
0/Cytokines; 0/Eicosanoids; 0/Fatty Acids; 0/NF-kappa B; 2508-19-2/Trinitrobenzenesulfonic Acid; 27415-26-5/8-epi-prostaglandin F2alpha; 463-40-1/alpha-Linolenic Acid; 551-11-1/Dinoprost; 70-18-8/Glutathione; 9008-11-1/Interferons; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 3.4.21.1/Chymotrypsin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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