File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1111/j.1600-079X.2004.00138.x
- Scopus: eid_2-s2.0-4344600602
- PMID: 15298666
- WOS: WOS:000223156200003
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Pretreatment with melatonin exerts anti-inflammatory effects against ischemia/reperfusion injury in a rat middle cerebral artery occlusion stroke model
Title | Pretreatment with melatonin exerts anti-inflammatory effects against ischemia/reperfusion injury in a rat middle cerebral artery occlusion stroke model |
---|---|
Authors | |
Keywords | Cerebral ischemia Cyclooxygenase-2 Glial fibrillary acidic protein Inflammation Ischemia/reperfusion injury Melatonin Myeloperoxidase Neuronal nitric oxide synthase |
Issue Date | 2004 |
Publisher | Blackwell 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? |
Abstract | Inflammatory 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 Identifier | http://hdl.handle.net/10722/78040 |
ISSN | 2023 Impact Factor: 8.3 2023 SCImago Journal Rankings: 2.194 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Pei, Z | en_HK |
dc.contributor.author | Cheung, RTF | en_HK |
dc.date.accessioned | 2010-09-06T07:38:30Z | - |
dc.date.available | 2010-09-06T07:38:30Z | - |
dc.date.issued | 2004 | en_HK |
dc.identifier.citation | Journal Of Pineal Research, 2004, v. 37 n. 2, p. 85-91 | en_HK |
dc.identifier.issn | 0742-3098 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/78040 | - |
dc.description.abstract | Inflammatory 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.language | eng | en_HK |
dc.publisher | Blackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI | en_HK |
dc.relation.ispartof | Journal of Pineal Research | en_HK |
dc.subject | Cerebral ischemia | - |
dc.subject | Cyclooxygenase-2 | - |
dc.subject | Glial fibrillary acidic protein | - |
dc.subject | Inflammation | - |
dc.subject | Ischemia/reperfusion injury | - |
dc.subject | Melatonin | - |
dc.subject | Myeloperoxidase | - |
dc.subject | Neuronal nitric oxide synthase | - |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Antioxidants - pharmacology | en_HK |
dc.subject.mesh | Brain - drug effects - metabolism - pathology | en_HK |
dc.subject.mesh | Cyclooxygenase 2 | en_HK |
dc.subject.mesh | Disease Models, Animal | en_HK |
dc.subject.mesh | Glial Fibrillary Acidic Protein - metabolism | en_HK |
dc.subject.mesh | Immunohistochemistry | en_HK |
dc.subject.mesh | Infarction, Middle Cerebral Artery - drug therapy - metabolism - pathology | en_HK |
dc.subject.mesh | Isoenzymes - metabolism | en_HK |
dc.subject.mesh | Male | en_HK |
dc.subject.mesh | Melatonin - pharmacology | en_HK |
dc.subject.mesh | Neurons - drug effects - metabolism - pathology | en_HK |
dc.subject.mesh | Neuroprotective Agents - pharmacology | en_HK |
dc.subject.mesh | Nitric Oxide Synthase - metabolism | en_HK |
dc.subject.mesh | Nitric Oxide Synthase Type I | en_HK |
dc.subject.mesh | Peroxidase - metabolism | en_HK |
dc.subject.mesh | Prostaglandin-Endoperoxide Synthases - metabolism | en_HK |
dc.subject.mesh | Rats | en_HK |
dc.subject.mesh | Rats, Sprague-Dawley | en_HK |
dc.subject.mesh | Reperfusion Injury - drug therapy - metabolism - pathology | en_HK |
dc.title | Pretreatment with melatonin exerts anti-inflammatory effects against ischemia/reperfusion injury in a rat middle cerebral artery occlusion stroke model | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+model | en_HK |
dc.identifier.email | Cheung, RTF:rtcheung@hku.hk | en_HK |
dc.identifier.authority | Cheung, RTF=rp00434 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1111/j.1600-079X.2004.00138.x | en_HK |
dc.identifier.pmid | 15298666 | en_HK |
dc.identifier.scopus | eid_2-s2.0-4344600602 | en_HK |
dc.identifier.hkuros | 99215 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-4344600602&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 37 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 85 | en_HK |
dc.identifier.epage | 91 | en_HK |
dc.identifier.isi | WOS:000223156200003 | - |
dc.publisher.place | Denmark | en_HK |
dc.identifier.scopusauthorid | Pei, Z=23051646800 | en_HK |
dc.identifier.scopusauthorid | Cheung, RTF=7202397498 | en_HK |
dc.identifier.issnl | 0742-3098 | - |