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Article: Influence of gender difference and gastritis on gastric ulcer formation in rats

TitleInfluence of gender difference and gastritis on gastric ulcer formation in rats
Authors
Issue Date2001
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH
Citation
Journal Of Gastroenterology And Hepatology, 2001, v. 16 n. 7, p. 740-747 How to Cite?
AbstractBackground: Male patients with gastritis are found to have a high risk of developing peptic ulcer diseases. However, how gastritis or gender difference affects gastric ulcer formation is unclear. The present study aimed to investigate the relationship between ethanol-induced acute gastritis and gastric ulcer formation in rats. Methods: Acute gastritis or gastric ulcer was induced in the rat stomach by 80% ethanol or 60% acetic acid, respectively. Rats were killed either with gastritis alone or thereafter at day 1, 3 or 6 after ulcer induction. The number of proliferating and apoptotic cells, the mucosal mucus and prostaglandin E2 (PGE2) level were also determined. Results: Male rats with acute gastritis potentiated gastric ulcer formation, while gastritis in female rats prevented ulceration. Female rats with gastritis had a significantly faster ulcer-healing rate. More apoptotic cells were found in the gastritis groups, but only the female gastritis group produced more proliferating cells and had a decrease in the apoptosis-over-proliferation ratio. The mucus level was higher in female rats after ulcer induction. Mucosal PGE2 level was higher in female rats with acute gastritis. Both mucus and PGE2 were increased during ulcer healing in both genders. Conclusions: This study shows that gender difference plays a role in the pathogenesis of ulcer formation. The number of cells with apoptosis or proliferation determines, in part, the gender difference on gastric ulcer formation in rats. Gastric PGE2 not only contributes to this process, but also together with gastric mucus participates in the ulcer-healing process in the stomach. © 2001 Blackwell Science Asia Pty Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/77436
ISSN
2015 Impact Factor: 3.322
2015 SCImago Journal Rankings: 1.190
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, ESLen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T07:31:53Z-
dc.date.available2010-09-06T07:31:53Z-
dc.date.issued2001en_HK
dc.identifier.citationJournal Of Gastroenterology And Hepatology, 2001, v. 16 n. 7, p. 740-747en_HK
dc.identifier.issn0815-9319en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77436-
dc.description.abstractBackground: Male patients with gastritis are found to have a high risk of developing peptic ulcer diseases. However, how gastritis or gender difference affects gastric ulcer formation is unclear. The present study aimed to investigate the relationship between ethanol-induced acute gastritis and gastric ulcer formation in rats. Methods: Acute gastritis or gastric ulcer was induced in the rat stomach by 80% ethanol or 60% acetic acid, respectively. Rats were killed either with gastritis alone or thereafter at day 1, 3 or 6 after ulcer induction. The number of proliferating and apoptotic cells, the mucosal mucus and prostaglandin E2 (PGE2) level were also determined. Results: Male rats with acute gastritis potentiated gastric ulcer formation, while gastritis in female rats prevented ulceration. Female rats with gastritis had a significantly faster ulcer-healing rate. More apoptotic cells were found in the gastritis groups, but only the female gastritis group produced more proliferating cells and had a decrease in the apoptosis-over-proliferation ratio. The mucus level was higher in female rats after ulcer induction. Mucosal PGE2 level was higher in female rats with acute gastritis. Both mucus and PGE2 were increased during ulcer healing in both genders. Conclusions: This study shows that gender difference plays a role in the pathogenesis of ulcer formation. The number of cells with apoptosis or proliferation determines, in part, the gender difference on gastric ulcer formation in rats. Gastric PGE2 not only contributes to this process, but also together with gastric mucus participates in the ulcer-healing process in the stomach. © 2001 Blackwell Science Asia Pty Ltd.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGHen_HK
dc.relation.ispartofJournal of Gastroenterology and Hepatologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshDinoprostone - analysisen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGastric Mucosa - chemistryen_HK
dc.subject.meshGastritis - complications - pathologyen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMucusen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshSex Factorsen_HK
dc.subject.meshStomach Ulcer - etiology - pathologyen_HK
dc.subject.meshWound Healingen_HK
dc.titleInfluence of gender difference and gastritis on gastric ulcer formation in ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0815-9319&volume=16&issue=7&spage=740&epage=747&date=2001&atitle=Influence+of+gender+difference+and+gastritis+on+gastric+ulcer+formation+in+ratsen_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1440-1746.2001.02506.xen_HK
dc.identifier.pmid11446881-
dc.identifier.scopuseid_2-s2.0-0035719055en_HK
dc.identifier.hkuros72196en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035719055&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume16en_HK
dc.identifier.issue7en_HK
dc.identifier.spage740en_HK
dc.identifier.epage747en_HK
dc.identifier.isiWOS:000179450800007-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridLiu, ESL=7202240071en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridCho, CH=14067000400en_HK

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