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Article: Morphine as a drug for stress ulcer prevention and healing in the stomach

TitleMorphine as a drug for stress ulcer prevention and healing in the stomach
Authors
KeywordsCell proliferation
Gastric ulcer
Morphine
Mucus
Myeloperoxidase
Stress
Issue Date2003
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2003, v. 460 n. 2-3, p. 177-182 How to Cite?
AbstractMorphine pretreatment protects against stress-induced gastric ulceration, however, the exact mechanism is still undefined. Interestingly, the effect of morphine on ulcer healing has not been investigated. In this report, we would like to study these effects in a defined stress ulcer model and to delineate a new implication for morphine to promote stress ulcer healing in rats. Our study showed that cold-restraint stress for 3 h induced hemorrhagic lesions and increased myeloperoxidase activity in the gastric mucosa. Stress also reduced the dimension of layer of periodic acid-Schiff reagent-stained cells in the gastric mucosa by about 50%. Morphine pretreatment (2 or 8 mg/kg, given intraperitoneally) at the time of stress dose-dependently reversed stress-induced gastric ulceration, increase of myeloperoxidase activity and reduction of thickness of mucus-stained cells in the gastric mucosa. Morphine treatment after stress (given at the end of a 3-h stress and also at 3 h thereafter) increased ulcer healing by reducing the ulcer size measured 24 h later. Such action was blocked by naloxone (8 mg/kg) given intraperitoneally 15 min before morphine treatment. Morphine also increased the number of cell proliferation and dimension of layer of cells stained for mucus but not the number of microvessels in the gastric mucosa. Moreover, the number of apoptotic cells was less evidenced in the morphine-treated rats. This study reports for the first time that morphine not only prevents stress ulceration but also promotes healing of stress ulcer through a defined mechanism. © 2003 Elsevier Science B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78348
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCho, CHen_HK
dc.contributor.authorWu, KKen_HK
dc.contributor.authorWu, Sen_HK
dc.contributor.authorWong, TMen_HK
dc.contributor.authorSo, WHLen_HK
dc.contributor.authorLiu, ESLen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorShin, VYen_HK
dc.contributor.authorYe, YNen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T07:41:53Z-
dc.date.available2010-09-06T07:41:53Z-
dc.date.issued2003en_HK
dc.identifier.citationEuropean Journal Of Pharmacology, 2003, v. 460 n. 2-3, p. 177-182en_HK
dc.identifier.issn0014-2999en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78348-
dc.description.abstractMorphine pretreatment protects against stress-induced gastric ulceration, however, the exact mechanism is still undefined. Interestingly, the effect of morphine on ulcer healing has not been investigated. In this report, we would like to study these effects in a defined stress ulcer model and to delineate a new implication for morphine to promote stress ulcer healing in rats. Our study showed that cold-restraint stress for 3 h induced hemorrhagic lesions and increased myeloperoxidase activity in the gastric mucosa. Stress also reduced the dimension of layer of periodic acid-Schiff reagent-stained cells in the gastric mucosa by about 50%. Morphine pretreatment (2 or 8 mg/kg, given intraperitoneally) at the time of stress dose-dependently reversed stress-induced gastric ulceration, increase of myeloperoxidase activity and reduction of thickness of mucus-stained cells in the gastric mucosa. Morphine treatment after stress (given at the end of a 3-h stress and also at 3 h thereafter) increased ulcer healing by reducing the ulcer size measured 24 h later. Such action was blocked by naloxone (8 mg/kg) given intraperitoneally 15 min before morphine treatment. Morphine also increased the number of cell proliferation and dimension of layer of cells stained for mucus but not the number of microvessels in the gastric mucosa. Moreover, the number of apoptotic cells was less evidenced in the morphine-treated rats. This study reports for the first time that morphine not only prevents stress ulceration but also promotes healing of stress ulcer through a defined mechanism. © 2003 Elsevier Science B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_HK
dc.relation.ispartofEuropean Journal of Pharmacologyen_HK
dc.rightsEuropean Journal of Pharmacology. Copyright © Elsevier BV.en_HK
dc.subjectCell proliferationen_HK
dc.subjectGastric ulceren_HK
dc.subjectMorphineen_HK
dc.subjectMucusen_HK
dc.subjectMyeloperoxidaseen_HK
dc.subjectStressen_HK
dc.subject.meshAnalgesics, Opioid - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshBlood Vessels - drug effectsen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshCold Temperatureen_HK
dc.subject.meshGastric Mucosa - blood supply - drug effects - pathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMorphine - pharmacologyen_HK
dc.subject.meshNaloxone - pharmacologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshStomach - drug effects - pathologyen_HK
dc.subject.meshStomach Ulcer - etiology - prevention & controlen_HK
dc.subject.meshStress, Physiological - complicationsen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshWound Healing - drug effectsen_HK
dc.titleMorphine as a drug for stress ulcer prevention and healing in the stomachen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-2999&volume=460&spage=177&epage=182&date=2003&atitle=Morphine+as+a+drug+for+stress+ulcer+prevention+and+healing+in+the+stomachen_HK
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0014-2999(02)02922-9en_HK
dc.identifier.pmid12559379-
dc.identifier.scopuseid_2-s2.0-12244271045en_HK
dc.identifier.hkuros82615en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-12244271045&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume460en_HK
dc.identifier.issue2-3en_HK
dc.identifier.spage177en_HK
dc.identifier.epage182en_HK
dc.identifier.isiWOS:000180963700013-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridCho, CH=7403100461en_HK
dc.identifier.scopusauthoridWu, KK=36991042600en_HK
dc.identifier.scopusauthoridWu, S=7408443898en_HK
dc.identifier.scopusauthoridWong, TM=36839495300en_HK
dc.identifier.scopusauthoridSo, WHL=7004974020en_HK
dc.identifier.scopusauthoridLiu, ESL=7202240071en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridShin, VY=7003491170en_HK
dc.identifier.scopusauthoridYe, YN=7401627402en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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