title: [Comparative study of novel therapeutic possibilities in animal experimental model of inflammatory bowel disease].
abstract: BACKGROUND
  The consequence of inflammatory bowel diseases (IBD) is cytokine-mediated severe local tissue damage. Our aim was to determine the extent of inflammatory response and to influence the morphologic changes during the subacute phase of trinitro-benzene sulfonic acid (TNBS)-induced experimental colitis by oral phosphatidylcholine (PC) and N-methyl-D-aspartate (NMDA) receptor antagonist kynurenic acid therapy.
  
  
  METHODS
  Sprague-Dawley rats were randomized to control, untreated colitis (ic TNBS), colitis fed with 2% PC-containing diet (3 days pre-treatment +3 days treatment after TNBS induction), colitis with kynurenic acid treatment (on day 6, n = 7) groups. The colitis was characterized by tissue myeloperoxidase and plasma TNF-alpha levels, the extent of tissue damage, structural changes in microvasculature (FITC-dextran staining) and mucosal injury (acridine orange staining) were determined by in vivo confocal laser scanning endomicroscopy (Optiscan Five1, Australia) and conventional histology (hematoxyilin-eosin staining).
  
  
  RESULTS
  Significant elevation in myeloperoxidase and TNF-alpha levels with remarkable damage in epithelial structure was detected in the colitis group. Both treatment regimens significantly decreased the level of inflammatory activation but only PC pretreatment could preserve the number of goblet cells and the epithelial structure. Treatment with kynurenic acid did not alter the morphology changes.
  
  
  CONCLUSIONS
  Oral PC pretreatment is a promising possibility in the therapy of IBDs through decreasing inflammatory reaction and increasing the number of goblet cells.
authors.affiliation: Szegedi Tudományegyetem, Általános Orvostudományi Kar Gyermekklinika, Gyermeksebészeti Osztály Szeged.
authors.forename: Tamás
authors.initials: T
authors.lastname: Kovács
authors.forename: Gabriella
authors.initials: G
authors.lastname: Varga
authors.forename: Dániel
authors.initials: D
authors.lastname: Erces
authors.forename: Tünde
authors.initials: T
authors.lastname: Tőkés
authors.forename: László
authors.initials: L
authors.lastname: Tiszlavicz
authors.forename: Miklós
authors.initials: M
authors.lastname: Ghyczy
authors.forename: László
authors.initials: L
authors.lastname: Vécsei
authors.forename: Mihály
authors.initials: M
authors.lastname: Boros
authors.forename: József
authors.initials: J
authors.lastname: Kaszaki
mesh_terms: D000284:Administration, Oral; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D003092:Colitis / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D004195:Disease Models, Animal; D018691:Excitatory Amino Acid Antagonists / Q000008:administration & dosage / Q000494:pharmacology*; D007249:Inflammation / Q000188:drug therapy; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy; D007413:Intestinal Mucosa / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D007736:Kynurenic Acid / Q000494:pharmacology*; D008833:Microcirculation; D018613:Microscopy, Confocal; D009195:Peroxidase / Q000378:metabolism; D010713:Phosphatidylcholines / Q000008:administration & dosage / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*; D014302:Trinitrobenzenesulfonic Acid; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D018691:Excitatory Amino Acid Antagonists; D010713:Phosphatidylcholines; D016194:Receptors, N-Methyl-D-Aspartate; D014409:Tumor Necrosis Factor-alpha; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase; D007736:Kynurenic Acid