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Article: Nonsteroidal antiinflammatory drugs could reverse Helicobacter pylori- induced apoptosis and proliferation in gastric epithelial cells

TitleNonsteroidal antiinflammatory drugs could reverse Helicobacter pylori- induced apoptosis and proliferation in gastric epithelial cells
Authors
Issue Date1998
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116
Citation
Digestive Diseases And Sciences, 1998, v. 43 n. 9, p. 1957-1963 How to Cite?
AbstractIt remains controversial whether the harmful effects of Helicobacter pylori (Hp) and nonsteroidal antiinflammatory drugs (NSAIDs) are additive. We studied the effects of Hp (virulent and nonvirulent strains) and NSAIDs, alone or in combination, on apoptosis and proliferation of gastric epithelial cells in nonulcer dyspepsia (NUD) patients. Forty-four (25 Hp-positive and 19 Hp-negative) consecutive Chinese NUD patients with rheumatoid arthritis who had taken continuously NSAIDs for more than three months were recruited for this study. Another 41 (20 Hp-positive and 21 Hp-negative) NUD patients not on any NSAIDs were included as controls. All patients underwent a gastroscopy examination and gastric biopsies. Hp infection was confirmed by CLOtest, anti-Hp ELISA, and [ 13C]urea breath test. The CagA status was determined by the anti-CagA antibody assay. The degree of gastritis, apoptosis, and proliferation indices were determined with H and E staining, terminal uridine deoxynucleotidyl nick end-labeling (TUNEL), and proliferating cell nuclear antigen (PCNA) immunostaining methods, respectively. A significantly higher apoptosis was observed in subjects who had Hp infection or had been consuming NSAIDS when compared with the controls. Unlike NSAID-treated subjects, patients with Hp infection were shown to have significantly enhanced cell proliferation. However, the increased apoptosis and proliferation in Hp- positive subjects were reversed by also taking NSAIDs. No correlation was found between apoptosis and proliferation in all the study groups. There was no association found between CagA expression or degree of gastritis with cell proliferation or apoptosis. It was demonstrated at the cellular level that NSAIDs could abrogate apoptosis or proliferation effects induced by Hp. Furthermore, the latter effects appeared not to be influenced by the virulent nature of the Hp strains.
Persistent Identifierhttp://hdl.handle.net/10722/162219
ISSN
2015 Impact Factor: 2.516
2015 SCImago Journal Rankings: 0.995
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhu, GHen_US
dc.contributor.authorYang, XLen_US
dc.contributor.authorLai, KCen_US
dc.contributor.authorChing, CKen_US
dc.contributor.authorWong, BCYen_US
dc.contributor.authorYuen, STen_US
dc.contributor.authorHo, Jen_US
dc.contributor.authorLam, SKen_US
dc.date.accessioned2012-09-05T05:18:12Z-
dc.date.available2012-09-05T05:18:12Z-
dc.date.issued1998en_US
dc.identifier.citationDigestive Diseases And Sciences, 1998, v. 43 n. 9, p. 1957-1963en_US
dc.identifier.issn0163-2116en_US
dc.identifier.urihttp://hdl.handle.net/10722/162219-
dc.description.abstractIt remains controversial whether the harmful effects of Helicobacter pylori (Hp) and nonsteroidal antiinflammatory drugs (NSAIDs) are additive. We studied the effects of Hp (virulent and nonvirulent strains) and NSAIDs, alone or in combination, on apoptosis and proliferation of gastric epithelial cells in nonulcer dyspepsia (NUD) patients. Forty-four (25 Hp-positive and 19 Hp-negative) consecutive Chinese NUD patients with rheumatoid arthritis who had taken continuously NSAIDs for more than three months were recruited for this study. Another 41 (20 Hp-positive and 21 Hp-negative) NUD patients not on any NSAIDs were included as controls. All patients underwent a gastroscopy examination and gastric biopsies. Hp infection was confirmed by CLOtest, anti-Hp ELISA, and [ 13C]urea breath test. The CagA status was determined by the anti-CagA antibody assay. The degree of gastritis, apoptosis, and proliferation indices were determined with H and E staining, terminal uridine deoxynucleotidyl nick end-labeling (TUNEL), and proliferating cell nuclear antigen (PCNA) immunostaining methods, respectively. A significantly higher apoptosis was observed in subjects who had Hp infection or had been consuming NSAIDS when compared with the controls. Unlike NSAID-treated subjects, patients with Hp infection were shown to have significantly enhanced cell proliferation. However, the increased apoptosis and proliferation in Hp- positive subjects were reversed by also taking NSAIDs. No correlation was found between apoptosis and proliferation in all the study groups. There was no association found between CagA expression or degree of gastritis with cell proliferation or apoptosis. It was demonstrated at the cellular level that NSAIDs could abrogate apoptosis or proliferation effects induced by Hp. Furthermore, the latter effects appeared not to be influenced by the virulent nature of the Hp strains.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116en_US
dc.relation.ispartofDigestive Diseases and Sciencesen_US
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - Therapeutic Useen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCell Division - Drug Effectsen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshDyspepsia - Drug Therapy - Microbiology - Pathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGastric Mucosa - Drug Effects - Microbiology - Pathologyen_US
dc.subject.meshGastritis - Drug Therapy - Microbiology - Pathologyen_US
dc.subject.meshHelicobacter Infections - Drug Therapy - Microbiology - Pathologyen_US
dc.subject.meshHelicobacter Pylorien_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshProspective Studiesen_US
dc.subject.meshTreatment Outcomeen_US
dc.titleNonsteroidal antiinflammatory drugs could reverse Helicobacter pylori- induced apoptosis and proliferation in gastric epithelial cellsen_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.doi10.1023/A:1018830408397en_US
dc.identifier.pmid9753258-
dc.identifier.scopuseid_2-s2.0-0031671840en_US
dc.identifier.hkuros39140-
dc.identifier.volume43en_US
dc.identifier.issue9en_US
dc.identifier.spage1957en_US
dc.identifier.epage1963en_US
dc.identifier.isiWOS:000075997300006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridZhu, GH=7402633170en_US
dc.identifier.scopusauthoridYang, XL=8878501600en_US
dc.identifier.scopusauthoridLai, KC=7402135595en_US
dc.identifier.scopusauthoridChing, CK=7102130825en_US
dc.identifier.scopusauthoridWong, BCY=7402023340en_US
dc.identifier.scopusauthoridYuen, ST=7103160927en_US
dc.identifier.scopusauthoridHo, J=15029093800en_US
dc.identifier.scopusauthoridLam, SK=7402279473en_US

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