[Comparative study of novel therapeutic possibilities in animal experimental model of inflammatory bowel disease]

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.

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).

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.

Oral PC pretreatment is a promising possibility in the therapy of IBDs through decreasing inflammatory reaction and increasing the number of goblet cells.