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Influence of Topical Rectal Application of Drugs on Dextran Sulfate-Induced Colitis in Rats

Influence of Topical Rectal Application of Drugs on Dextran Sulfate-Induced Colitis in Rats A rat model of colitis [dextran sulfate (DSS)]was used to study the permeation of Evans blue (EB) fromthe lumen into the wall of proximal and distal colonicloops after exposure to the dye for 2 hr. Topical application of drugs used in human ulcerativecolitis (lidocaine, mesalazine, prednisolone, orsucralfate) was given daily during induction of colitisto protect the mucosa. The mucosal changes wereevaluated with special regard to peptidergic innervation[substance P (SP) and neuropeptide Y (NPY)], invasion ofantigen-presenting polydendritic cells, andmucin-containing goblet cells. DSS-treatment caused a significantly increased permeation of EB. Inthe proximal loops a significant inhibition was obtainedafter treatment with lidocaine, prednisolone, orsucralfate. In the distal loops only treatment with lidocaine had a preventive effect.Immunocytochemically there was a clear hyperplasia ofboth mucosal SP- and NPY-immunoreactive nerve fibers inregions with crypt abnormalities. In these regions alsomost of the goblet cells were devoid of mucus. Likethe changes in permeation, these morphological changeswere most prominent in the distal loops. With inductionof colitis, the mucosa and lamina propria were invaded by polydendritic cells; the visualscore was markedly decreased in the proximal loopstreated with lidocaine, prednisolone, or sucralfate. Inthe distal loops similar effects were obtained after treatment with lidocaine or prednisolone.Prevention of the influx of antigens in both loops afterlidocaine treatment with reduced recruitment ofpolydendritic cells into the lamina propria issuggested. The nerve hyperplasia may thus be secondary toluminal challenge with antigens during induction ofcolitis. The discrepancy between increased permeationand absence of polydendritic cell response in the distal loops after prednisolone may reflectseparate actions of steroids on the intestinalepithelium and the immune cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Digestive Diseases and Sciences Springer Journals

Influence of Topical Rectal Application of Drugs on Dextran Sulfate-Induced Colitis in Rats

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References (48)

Publisher
Springer Journals
Copyright
Copyright © 1997 by Plenum Publishing Corporation
Subject
Medicine & Public Health; Gastroenterology; Hepatology; Oncology; Transplant Surgery; Biochemistry, general
ISSN
0163-2116
eISSN
1573-2568
DOI
10.1023/A:1018880501437
Publisher site
See Article on Publisher Site

Abstract

A rat model of colitis [dextran sulfate (DSS)]was used to study the permeation of Evans blue (EB) fromthe lumen into the wall of proximal and distal colonicloops after exposure to the dye for 2 hr. Topical application of drugs used in human ulcerativecolitis (lidocaine, mesalazine, prednisolone, orsucralfate) was given daily during induction of colitisto protect the mucosa. The mucosal changes wereevaluated with special regard to peptidergic innervation[substance P (SP) and neuropeptide Y (NPY)], invasion ofantigen-presenting polydendritic cells, andmucin-containing goblet cells. DSS-treatment caused a significantly increased permeation of EB. Inthe proximal loops a significant inhibition was obtainedafter treatment with lidocaine, prednisolone, orsucralfate. In the distal loops only treatment with lidocaine had a preventive effect.Immunocytochemically there was a clear hyperplasia ofboth mucosal SP- and NPY-immunoreactive nerve fibers inregions with crypt abnormalities. In these regions alsomost of the goblet cells were devoid of mucus. Likethe changes in permeation, these morphological changeswere most prominent in the distal loops. With inductionof colitis, the mucosa and lamina propria were invaded by polydendritic cells; the visualscore was markedly decreased in the proximal loopstreated with lidocaine, prednisolone, or sucralfate. Inthe distal loops similar effects were obtained after treatment with lidocaine or prednisolone.Prevention of the influx of antigens in both loops afterlidocaine treatment with reduced recruitment ofpolydendritic cells into the lamina propria issuggested. The nerve hyperplasia may thus be secondary toluminal challenge with antigens during induction ofcolitis. The discrepancy between increased permeationand absence of polydendritic cell response in the distal loops after prednisolone may reflectseparate actions of steroids on the intestinalepithelium and the immune cells.

Journal

Digestive Diseases and Sciences – Springer Journals

Published: Oct 15, 2004

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