| Effect of ebrotidine on gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide. | |
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MedLine Citation:
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PMID: 10574469 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Helicobacter pylori lipopolysaccharide is a primary virulence factor responsible for eliciting acute mucosal inflammatory responses associated with H. pylori infection. In this study, we applied the animal model of H. pylori lipopolysaccharide-induced acute gastritis to assess the effect of antiulcer agent, ebrotidine, on the gastric mucosal inflammatory responses by analyzing the interplay between the activity of a key apoptotic caspase, caspase-3, epithelial cell apoptosis, and the expression of inducible nitric oxide synthase (NOS-2). METHODS: Rats, pretreated twice daily with ebrotidine at 100 mg/kg, or the vehicle, were subjected to intragastric application of H. pylori lipopolysaccharide at 50 microg/animal, and after 4 additional days on the antiulcer drug or vehicle regimen their mucosal tissue used for histologic assessment, assays of epithelial cells apoptosis, and the measurements of caspase-3 and NOS-2 activities. RESULTS: In the absence of antiulcer agent, H. pylori lipopolysaccharide induced acute reaction characterized by the inflammatory infiltration of the lamina propria, hyperemia, and epithelial hemorrhage. This was accompanied by an 11.2-fold increase in epithelial cell apoptosis, a 6.5-fold induction in mucosal expression of NOS-2, and a 5.4-fold increase in caspase-3 activity. Treatment with H2-receptor antagonist ebrotidine, also known for its gastroprotective effects, produced a 50.9% reduction in the extent of mucosal inflammatory changes elicited by H. pylori lipopolysaccharide and an 82.5% decrease in the epithelial cells apoptosis, while the activity of caspase-3 decreased by 33.7% and that of NOS-2 showed a 72.8% decline. CONCLUSIONS: The findings implicate caspase-3 involvement in gastric mucosal inflammatory responses to H. pylori lipopolysaccharide, and point towards participation of NOS-2 in the amplification of the cell death-signaling cascade. Our study also demonstrate that ebrotidine exerts modulatory effect on the H. pylori-induced mucosal inflammatory responses by interfering with the events propagated by NOS-2 and caspase-3. |
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Authors:
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B L Slomiany; J Piotrowski; A Slomiany |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of physiology and pharmacology : an official journal of the Polish Physiological Society Volume: 50 ISSN: 0867-5910 ISO Abbreviation: J. Physiol. Pharmacol. Publication Date: 1999 Sep |
Date Detail:
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Created Date: 1999-12-09 Completed Date: 1999-12-09 Revised Date: 2003-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9114501 Medline TA: J Physiol Pharmacol Country: POLAND |
Other Details:
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Languages: eng Pagination: 391-404 Citation Subset: IM |
Affiliation:
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Research Center, University of Medicine and Dentistry of New Jersey, Newark 07103-2400, USA. slomiabr@umdnj.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Disease Animals Anti-Ulcer Agents / pharmacology* Benzenesulfonates / pharmacology* Disease Models, Animal Gastric Mucosa / drug effects, enzymology, pathology* Gastritis / drug therapy*, microbiology, pathology Helicobacter Infections / drug therapy*, microbiology, pathology Helicobacter pylori* Lipopolysaccharides / toxicity* Rats Rats, Sprague-Dawley Thiazoles / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Anti-Ulcer Agents; 0/Benzenesulfonates; 0/Lipopolysaccharides; 0/Thiazoles; 100981-43-9/ebrotidine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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