title: Dietary α-linolenic acid-rich formula reduces adhesion molecules in rats with experimental colitis.
abstract: OBJECTIVE
  The ω-3 polyunsaturated fatty acid therapy in inflammatory bowel disease is focused on the effects on fish oil-derived polyunsaturated fatty acids. We speculated that a vegetal oil rich in α-linolenic acid (ALA) might also inhibit colitis. Therefore, we evaluated whether dietary ALA would decrease the expression of adhesion molecules by inducing the protective enzyme heme oxygenase-1 (HO-1) in a rat colitis model.
  
  
  METHODS
  Colitis was induced at day 0 by an intrarectal injection of 2-4-6-trinitrobenzen sulfonic acid (TNBS), whereas control rats received the vehicle. Rats were fed an ALA-rich formula 450 mg · kg⁻¹ · d⁻¹, whereas the other colitic group (TNBS) and the control group were fed an isocaloric corn oil formula for 14 d (from day -7 to day 7). The colonic expressions of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), vascular endothelial growth factor A receptor-2 (VEGFR2), and HO-1 were studied by immunohistochemistry.
  
  
  RESULTS
  The ALA-rich diet significantly decreased the expression of ICAM-1, VCAM-1, and VEGFR-2 compared the TNBS group, but it did not affect the expression of HO-1.
  
  
  CONCLUSIONS
  A vegetal ALA-rich formula decreases the expression of ICAM-1, VCAM-1, and VEGFR-2 and independently of HO-1 in rats with TNBS-induced colitis. Further studies are required to evaluate its therapeutic potential in inflammatory bowel disease as an alternative to fish oil.
authors.affiliation: Medicine University, Institute of Biomedical Research, Rouen, France.
authors.forename: Ayman
authors.initials: A
authors.lastname: Ibrahim
authors.forename: Moutaz
authors.initials: M
authors.lastname: Aziz
authors.forename: Aktham
authors.initials: A
authors.lastname: Hassan
authors.forename: Khaly
authors.initials: K
authors.lastname: Mbodji
authors.forename: Elodie
authors.initials: E
authors.lastname: Collasse
authors.forename: Moïse
authors.initials: M
authors.lastname: Coëffier
authors.forename: Frédéric
authors.initials: F
authors.lastname: Bounoure
authors.forename: Guillaume
authors.initials: G
authors.lastname: Savoye
authors.forename: Pierre
authors.initials: P
authors.lastname: Déchelotte
authors.forename: Rachel
authors.initials: R
authors.lastname: Marion-Letellier
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000032:analysis / Q000737:chemistry / Q000627:therapeutic use; D019607:Brassicaceae / Q000737:chemistry; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D003092:Colitis / Q000178:diet therapy / Q000473:pathology / Q000517:prevention & control*; D003106:Colon / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019587:Dietary Supplements / Q000032:analysis; D004195:Disease Models, Animal; D015536:Down-Regulation; D051547:Heme Oxygenase-1 / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D010938:Plant Oils / Q000737:chemistry / Q000627:therapeutic use; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000378:metabolism; D017962:alpha-Linolenic Acid / Q000032:analysis / Q000627:therapeutic use*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015815:Cell Adhesion Molecules; D010938:Plant Oils; D019010:Vascular Cell Adhesion Molecule-1; D017962:alpha-Linolenic Acid; D018799:Intercellular Adhesion Molecule-1; D051547:Heme Oxygenase-1; D040301:Vascular Endothelial Growth Factor Receptor-2