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Article: Pretreatment with melatonin exerts anti-inflammatory effects against ischemia/reperfusion injury in a rat middle cerebral artery occlusion stroke model

TitlePretreatment with melatonin exerts anti-inflammatory effects against ischemia/reperfusion injury in a rat middle cerebral artery occlusion stroke model
Authors
Issue Date2004
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI
Citation
Journal Of Pineal Research, 2004, v. 37 n. 2, p. 85-91 How to Cite?
AbstractInflammatory response following cerebral ischemia/reperfusion plays a key pathogenic role in ischemic cerebral damage. Nitric oxide (NO), cyclooxygenase-2 (COX-2) and myeloperoxidase (MPO) are important inflammatory mediators. Neuronal NO synthase (nNOS) is a major initial source of excessive NO during ischemia/reperfusion. Induction of COX-2 and infiltration of polymorphonuclear cells expressing MPO are critical factors in delayed inflammatory damage. Previously, we demonstrated that administration of melatonin before ischemia significantly reduced the infarct volume in a rat middle cerebral artery occlusion (MCAO) stroke model. In this study, we examined the effect of pretreatment with melatonin at 5 mg/kg on the immunoreactivity (ir) for nNOS, COX-2, MPO, and glial fibrillary acidic protein (GFAP) at 24, 48, and 72 hr after right-sided endovascular MCAO for 1 hr in adult male Sprague-Dawley rats. Melatonin did not affect the hemodynamic parameters. When compared with rats with sham MCAO, ischemia/reperfusion led to an ipsilateral increase in cells with positive ir for nNOS (similar at all times) and in ir-GFAP (similar at all times). Ischemia/ reperfusion led to appearance of cells with positive ir for COX-2 (greatest at 24 hr with a tendency to increase again at 72 hr) or MPO (greatest at 24 hr). A single dose of melatonin significantly lessened the ipsilateral increase in cells with positive ir for nNOS, COX-2 or MPO, but did not influence the ipsilateral change in ir-GFAP. Our results suggest that melatonin treatment mediates neuroprotection against ischemia/reperfusion injury partly via inhibition of the consequential inflammatory response.
Persistent Identifierhttp://hdl.handle.net/10722/78040
ISSN
2015 Impact Factor: 9.314
2015 SCImago Journal Rankings: 2.655
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPei, Zen_HK
dc.contributor.authorCheung, RTFen_HK
dc.date.accessioned2010-09-06T07:38:30Z-
dc.date.available2010-09-06T07:38:30Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Pineal Research, 2004, v. 37 n. 2, p. 85-91en_HK
dc.identifier.issn0742-3098en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78040-
dc.description.abstractInflammatory response following cerebral ischemia/reperfusion plays a key pathogenic role in ischemic cerebral damage. Nitric oxide (NO), cyclooxygenase-2 (COX-2) and myeloperoxidase (MPO) are important inflammatory mediators. Neuronal NO synthase (nNOS) is a major initial source of excessive NO during ischemia/reperfusion. Induction of COX-2 and infiltration of polymorphonuclear cells expressing MPO are critical factors in delayed inflammatory damage. Previously, we demonstrated that administration of melatonin before ischemia significantly reduced the infarct volume in a rat middle cerebral artery occlusion (MCAO) stroke model. In this study, we examined the effect of pretreatment with melatonin at 5 mg/kg on the immunoreactivity (ir) for nNOS, COX-2, MPO, and glial fibrillary acidic protein (GFAP) at 24, 48, and 72 hr after right-sided endovascular MCAO for 1 hr in adult male Sprague-Dawley rats. Melatonin did not affect the hemodynamic parameters. When compared with rats with sham MCAO, ischemia/reperfusion led to an ipsilateral increase in cells with positive ir for nNOS (similar at all times) and in ir-GFAP (similar at all times). Ischemia/ reperfusion led to appearance of cells with positive ir for COX-2 (greatest at 24 hr with a tendency to increase again at 72 hr) or MPO (greatest at 24 hr). A single dose of melatonin significantly lessened the ipsilateral increase in cells with positive ir for nNOS, COX-2 or MPO, but did not influence the ipsilateral change in ir-GFAP. Our results suggest that melatonin treatment mediates neuroprotection against ischemia/reperfusion injury partly via inhibition of the consequential inflammatory response.en_HK
dc.languageengen_HK
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPIen_HK
dc.relation.ispartofJournal of Pineal Researchen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntioxidants - pharmacologyen_HK
dc.subject.meshBrain - drug effects - metabolism - pathologyen_HK
dc.subject.meshCyclooxygenase 2en_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshGlial Fibrillary Acidic Protein - metabolismen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshInfarction, Middle Cerebral Artery - drug therapy - metabolism - pathologyen_HK
dc.subject.meshIsoenzymes - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMelatonin - pharmacologyen_HK
dc.subject.meshNeurons - drug effects - metabolism - pathologyen_HK
dc.subject.meshNeuroprotective Agents - pharmacologyen_HK
dc.subject.meshNitric Oxide Synthase - metabolismen_HK
dc.subject.meshNitric Oxide Synthase Type Ien_HK
dc.subject.meshPeroxidase - metabolismen_HK
dc.subject.meshProstaglandin-Endoperoxide Synthases - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReperfusion Injury - drug therapy - metabolism - pathologyen_HK
dc.titlePretreatment with melatonin exerts anti-inflammatory effects against ischemia/reperfusion injury in a rat middle cerebral artery occlusion stroke modelen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0742-3098&volume=37&spage=85&epage=91&date=2004&atitle=Pretreatment+with+melatonin+exerts+anti-inflammatory+effects+against+ischemia/reperfusion+injury+in+a+rat+middle+cerebral+artery+occlusion+stroke+modelen_HK
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_HK
dc.identifier.authorityCheung, RTF=rp00434en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-079X.2004.00138.xen_HK
dc.identifier.pmid15298666en_HK
dc.identifier.scopuseid_2-s2.0-4344600602en_HK
dc.identifier.hkuros99215en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4344600602&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue2en_HK
dc.identifier.spage85en_HK
dc.identifier.epage91en_HK
dc.identifier.isiWOS:000223156200003-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridPei, Z=23051646800en_HK
dc.identifier.scopusauthoridCheung, RTF=7202397498en_HK

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