Both (n-3) and (n-6) fatty acids stimulate wound healing in the rat intestinal epithelial cell line, IEC-6

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 IE C-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 ac ids on growth of IEC-6 cultures. Incorporation of supplemental fatty acids into cellular phospholipid was examined by thin-layer chromatography combin ed with gas chromatography. The modulation of epithelial restitution was ex amined by razor blade wounding confluent IEC-6 monolayers grown in media su pplemented 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 epithelia l cell model at concentrations above 125 mu mol/L. The trans fatty acid, li noelaidate 18:2(n-6)trans, inhibited growth of IEC-6 cells at concentration s above 250 mu mol/L. Another trans fatty acid, elaidate 18:1(n-9)trans, wa s well-tolerated at concentrations as high as 500 mu mol/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 cellul ar migration in the IEC-6 model of wound healing. Eicosapentanoate, linolea te, 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 b y n-6 fatty acids back to control levels.