Non-steroidal anti-inflammatory drugs inhibitHelicobacter pylori-induced human neutrophil reactive oxygen metabolite productionin vitro

Autor:	Jones-Blackett S, Mark A. Hull, Jean E. Crabtree, Davies Gr
Rok vydání:	1999
Předmět:	chemistry.chemical_classification Reactive oxygen species Hepatology biology Metabolite Gastroenterology Helicobacter pylori Pharmacology N-Formylmethionine leucyl-phenylalanine biology.organism_classification Xanthine digestive system diseases Meclofenamic acid chemistry.chemical_compound Diclofenac chemistry Immunology medicine Pharmacology (medical) Xanthine oxidase medicine.drug
Zdroj:	Alimentary Pharmacology & Therapeutics. 13:1653-1661
ISSN:	0269-2813
DOI:	10.1046/j.1365-2036.1999.00670.x
Popis:	Background: Helicobacter pylori infection is associated with increased production of gastric mucosal reactive oxygen metabolites which have been implicated in mucosal damage and carcinogenesis. In vitro, neutrophils produce reactive oxygen metabolites following activation by H. pylori. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit neutrophil activation by several factors, e.g. N-formyl-methionyl-leucyl-phenyalanine (f-MLP). Aim: To examine the effect of NSAIDs on H. pylori-induced reactive oxygen metabolite production by human peripheral blood neutrophils. Methods: Neutrophils were stimulated by H. pylori (NCTC 11637) water extract or f-MLP in the presence or absence of NSAIDs. Reactive oxygen metabolite activity was measured by luminol-enhanced chemiluminescence. Results: H. pylori water extract stimulated a sevenfold increase in chemiluminescence which was inhibited dose-dependently by diclofenac. All six NSAIDs studied (at 10–4 M) significantly inhibited H. pylori-and f-MLP-stimulated neutrophil reactive oxygen metabolite production. Meclofenamic acid and diclofenac had the greatest inhibitory effects on both H. pylori and f-MLP-stimulated neutrophil reactive oxygen metabolite production. The inhibitory effects of other NSAIDs varied with the activation stimulus. NSAIDs did not quench reactive oxygen metabolites generated in a cell-free xanthine:xanthine oxidase assay. Conclusion: Several NSAIDs attenuate H. pylori-induced neutrophil reactive oxygen metabolites production in vitro. This may be relevant to a potential chemopreventative role in gastric cancer and to a possible lack of synergy between H. pylori and NSAID use regarding peptic ulceration.
Databáze:	OpenAIRE
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