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- Publisher Website: 10.1046/j.1440-1746.2001.02506.x
- Scopus: eid_2-s2.0-0035719055
- PMID: 11446881
- WOS: WOS:000179450800007
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Article: Influence of gender difference and gastritis on gastric ulcer formation in rats
Title | Influence of gender difference and gastritis on gastric ulcer formation in rats |
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Authors | |
Keywords | Apoptosis Ethanol Gastric ulcer Gastritis Proliferation |
Issue Date | 2001 |
Publisher | Wiley-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? |
Abstract | Background: 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 Identifier | http://hdl.handle.net/10722/77436 |
ISSN | 2023 Impact Factor: 3.7 2023 SCImago Journal Rankings: 1.179 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Liu, ESL | en_HK |
dc.contributor.author | Wong, BCY | en_HK |
dc.contributor.author | Cho, CH | en_HK |
dc.date.accessioned | 2010-09-06T07:31:53Z | - |
dc.date.available | 2010-09-06T07:31:53Z | - |
dc.date.issued | 2001 | en_HK |
dc.identifier.citation | Journal Of Gastroenterology And Hepatology, 2001, v. 16 n. 7, p. 740-747 | en_HK |
dc.identifier.issn | 0815-9319 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/77436 | - |
dc.description.abstract | Background: 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.language | eng | en_HK |
dc.publisher | Wiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH | en_HK |
dc.relation.ispartof | Journal of Gastroenterology and Hepatology | en_HK |
dc.subject | Apoptosis | - |
dc.subject | Ethanol | - |
dc.subject | Gastric ulcer | - |
dc.subject | Gastritis | - |
dc.subject | Proliferation | - |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Apoptosis | en_HK |
dc.subject.mesh | Dinoprostone - analysis | en_HK |
dc.subject.mesh | Female | en_HK |
dc.subject.mesh | Gastric Mucosa - chemistry | en_HK |
dc.subject.mesh | Gastritis - complications - pathology | en_HK |
dc.subject.mesh | Immunohistochemistry | en_HK |
dc.subject.mesh | Male | en_HK |
dc.subject.mesh | Mucus | en_HK |
dc.subject.mesh | Rats | en_HK |
dc.subject.mesh | Rats, Sprague-Dawley | en_HK |
dc.subject.mesh | Sex Factors | en_HK |
dc.subject.mesh | Stomach Ulcer - etiology - pathology | en_HK |
dc.subject.mesh | Wound Healing | en_HK |
dc.title | Influence of gender difference and gastritis on gastric ulcer formation in rats | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+rats | en_HK |
dc.identifier.email | Wong, BCY:bcywong@hku.hk | en_HK |
dc.identifier.authority | Wong, BCY=rp00429 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1046/j.1440-1746.2001.02506.x | en_HK |
dc.identifier.pmid | 11446881 | - |
dc.identifier.scopus | eid_2-s2.0-0035719055 | en_HK |
dc.identifier.hkuros | 72196 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0035719055&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 16 | en_HK |
dc.identifier.issue | 7 | en_HK |
dc.identifier.spage | 740 | en_HK |
dc.identifier.epage | 747 | en_HK |
dc.identifier.isi | WOS:000179450800007 | - |
dc.publisher.place | Australia | en_HK |
dc.identifier.scopusauthorid | Liu, ESL=7202240071 | en_HK |
dc.identifier.scopusauthorid | Wong, BCY=7402023340 | en_HK |
dc.identifier.scopusauthorid | Cho, CH=14067000400 | en_HK |
dc.identifier.issnl | 0815-9319 | - |