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Article: Prostaglandin, tumor necrosis factor α and neutrophils: Causative relationship in indomethacin-induced stomach injuries

TitleProstaglandin, tumor necrosis factor α and neutrophils: Causative relationship in indomethacin-induced stomach injuries
Authors
Issue Date1998
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 1998, v. 348 n. 2-3, p. 257-263 How to Cite?
AbstractTumor necrosis factor alpha (TNF-α) has been suggested to play a critical role in indomethacin-induced gastric mucosal damage, so we evaluated its mucosal level and its relationship with prostaglandin E 2 and neutrophils in indomethacin-induced gastric mucosal injury in rats. Indomethacin caused a time- and dose-dependent increase in gastric mucosal erosion, which was accompanied by a reduction in prostaglandin E 2 followed by an increase in TNF-α level and neutrophil infiltration in the gastric mucosa. Pretreatment with exogenous prostaglandin E 2 totally abolished indomethacin-induced gastric mucosal injury and the TNF-α increase. Depletion of neutrophils by methotrexate or reduction of TNF-α concentration by pentoxifylline markedly reduced indomethacin-induced mucosal damage. Pentoxifylline but not methotrexate prevented the increase in mucosal TNF-α level induced by indomethacin. It is suggested that depletion of prostaglandin E 2 followed by an increase of TNF-α production and neutrophil infiltration in the gastric mucosa are important sequential processes in indomethacin-induced ulceration. Prevention of one of these processes would inhibit ulcer formation.
Persistent Identifierhttp://hdl.handle.net/10722/162261
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDing, SZen_US
dc.contributor.authorLam, SKen_US
dc.contributor.authorYuen, STen_US
dc.contributor.authorWong, BCYen_US
dc.contributor.authorHui, WMen_US
dc.contributor.authorHo, Jen_US
dc.contributor.authorGuo, Xen_US
dc.contributor.authorCho, CHen_US
dc.date.accessioned2012-09-05T05:18:29Z-
dc.date.available2012-09-05T05:18:29Z-
dc.date.issued1998en_US
dc.identifier.citationEuropean Journal Of Pharmacology, 1998, v. 348 n. 2-3, p. 257-263en_US
dc.identifier.issn0014-2999en_US
dc.identifier.urihttp://hdl.handle.net/10722/162261-
dc.description.abstractTumor necrosis factor alpha (TNF-α) has been suggested to play a critical role in indomethacin-induced gastric mucosal damage, so we evaluated its mucosal level and its relationship with prostaglandin E 2 and neutrophils in indomethacin-induced gastric mucosal injury in rats. Indomethacin caused a time- and dose-dependent increase in gastric mucosal erosion, which was accompanied by a reduction in prostaglandin E 2 followed by an increase in TNF-α level and neutrophil infiltration in the gastric mucosa. Pretreatment with exogenous prostaglandin E 2 totally abolished indomethacin-induced gastric mucosal injury and the TNF-α increase. Depletion of neutrophils by methotrexate or reduction of TNF-α concentration by pentoxifylline markedly reduced indomethacin-induced mucosal damage. Pentoxifylline but not methotrexate prevented the increase in mucosal TNF-α level induced by indomethacin. It is suggested that depletion of prostaglandin E 2 followed by an increase of TNF-α production and neutrophil infiltration in the gastric mucosa are important sequential processes in indomethacin-induced ulceration. Prevention of one of these processes would inhibit ulcer formation.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_US
dc.relation.ispartofEuropean Journal of Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - Toxicityen_US
dc.subject.meshCyclooxygenase Inhibitors - Toxicityen_US
dc.subject.meshDinoprostone - Analysis - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshGastric Mucosa - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshIndomethacin - Toxicityen_US
dc.subject.meshLeukocyte Counten_US
dc.subject.meshMaleen_US
dc.subject.meshMethotrexate - Pharmacologyen_US
dc.subject.meshNeutrophils - Drug Effectsen_US
dc.subject.meshNucleic Acid Synthesis Inhibitors - Pharmacologyen_US
dc.subject.meshPentoxifylline - Pharmacologyen_US
dc.subject.meshPhosphodiesterase Inhibitors - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshStomach Ulcer - Blood - Etiology - Prevention & Controlen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Analysis - Metabolismen_US
dc.titleProstaglandin, tumor necrosis factor α and neutrophils: Causative relationship in indomethacin-induced stomach injuriesen_US
dc.typeArticleen_US
dc.identifier.emailWong, BCY:bcywong@hku.hken_US
dc.identifier.authorityWong, BCY=rp00429en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0014-2999(98)00162-9en_US
dc.identifier.pmid9652341-
dc.identifier.scopuseid_2-s2.0-0032496073en_US
dc.identifier.hkuros32577-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032496073&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume348en_US
dc.identifier.issue2-3en_US
dc.identifier.spage257en_US
dc.identifier.epage263en_US
dc.identifier.isiWOS:000074031700014-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridDing, SZ=55255080600en_US
dc.identifier.scopusauthoridLam, SK=7402279473en_US
dc.identifier.scopusauthoridYuen, ST=7103160927en_US
dc.identifier.scopusauthoridWong, BCY=7402023340en_US
dc.identifier.scopusauthoridHui, WM=36900809400en_US
dc.identifier.scopusauthoridHo, J=7402650285en_US
dc.identifier.scopusauthoridGuo, X=55202826300en_US
dc.identifier.scopusauthoridCho, CH=14067000400en_US

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