title: Both (n-3) and (n-6) fatty acids stimulate wound healing in the rat intestinal epithelial cell line, IEC-6.
abstract: The control of proliferation and epithelial restitution are processes that are poorly understood. The effects of (n-3), (n-6) and trans fatty acids on proliferation of subconfluent IEC-6 cultures and restitution of wounded IEC-6 monolayers were investigated. Incorporation of supplemented fatty acids into cellular phospholipid was also assessed. Sulforhodamine B protein dye binding assay was utilized to assess the proliferative effects of fatty acids on growth of IEC-6 cultures. Incorporation of supplemental fatty acids into cellular phospholipid was examined by thin-layer chromatography combined with gas chromatography. The modulation of epithelial restitution was examined by razor blade wounding confluent IEC-6 monolayers grown in media supplemented with various fatty acids. Inhibition of eicosanoid synthesis by indomethacin during the wounding assay was also assessed. Both (n-3) and (n-6) fatty acids significantly inhibited growth of this intestinal epithelial cell model at concentrations above 125 micromol/L. The trans fatty acid, linoelaidate 18:2(n-6)trans, inhibited growth of IEC-6 cells at concentrations above 250 micromol/L. Another trans fatty acid, elaidate 18:1(n-9)trans, was well-tolerated at concentrations as high as 500 micromol/L. Eicosapentanoic 20:5(n-3), linoleic 18:2(n-6), alpha-linolenic 18:3(n-3), gamma-linolenic 18:3(n-6) and arachidonic 20:4(n-6) acids all significantly enhanced cellular migration in the IEC-6 model of wound healing. Eicosapentanoate, linoleate, alpha-linolenate, gamma-linolenate and arachidonate are all capable of improving reconstitution of epithelial integrity following mucosal injury. Inhibition of eicosanoid synthesis reduced the enhancement of restitution by n-6 fatty acids back to control levels.
authors.affiliation: Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1.
authors.forename: D J
authors.initials: DJ
authors.lastname: Ruthig
authors.forename: K A
authors.initials: KA
authors.lastname: Meckling-Gill
mesh_terms: D000818:Animals; D002460:Cell Line; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D002478:Cells, Cultured; D002849:Chromatography, Gas; D002853:Chromatography, Liquid; D015525:Fatty Acids, Omega-3 / Q000378:metabolism / Q000494:pharmacology* / Q000627:therapeutic use; D043371:Fatty Acids, Omega-6; D005231:Fatty Acids, Unsaturated / Q000378:metabolism / Q000494:pharmacology* / Q000627:therapeutic use; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6; D005231:Fatty Acids, Unsaturated; D010743:Phospholipids