File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Melatonin reduces nitric oxide level during ischemia but not blood-brain barrier breakdown during reperfusion in a rat middle cerebral artery occlusion stroke model

TitleMelatonin reduces nitric oxide level during ischemia but not blood-brain barrier breakdown during reperfusion in a rat middle cerebral artery occlusion stroke model
Authors
Issue Date2003
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI
Citation
Journal Of Pineal Research, 2003, v. 34 n. 2, p. 110-118 How to Cite?
AbstractMelatonin is a potent antioxidant and free radical scavenger. Previously, we showed that a single injection of melatonin before ischemia significantly reduced the infarct volume in both permanent and 3-hr middle cerebral artery occlusion (MCAO) rat stroke models. Nitric oxide (NO) and other free radicals play an important role in the pathogenesis of cerebral ischemia, and they have been postulated to mediate the breakdown of the blood-brain barrier (BBB) during ischemia. In this study, we evaluated the influence of melatonin, given at 30 min before MCAO, on brain NO concentration and BBB breakdown. Brain NO concentration was measured at 15 min of MCAO using electron paramagnetic resonance spectroscopy. BBB breakdown at 3 hr of reperfusion following 3 hr of MCAO was assessed using Evans blue extravasation. The relative brain NO concentration was increased to 141.69 ± 9.71% (mean ± S.E.M.; n = 9) at 15 min of MCAO. Treatment with melatonin at 1.5, 5, or 50 mg/kg significantly reduced the brain NO concentration to 104.20 ± 11.20% (n = 8), 55.67 ± 5.58% (n = 11), and 104.86 ± 12.56% (n = 9), respectively. Melatonin at 5 mg/kg did not affect Evans blue extravasation. Our results suggest that a single injection of melatonin protects against focal cerebral ischemia partly via inhibition of ischemia-induced NO production and that this regimen does not prevent BBB breakdown following ischemia-reperfusion.
Persistent Identifierhttp://hdl.handle.net/10722/162678
ISSN
2015 Impact Factor: 9.314
2015 SCImago Journal Rankings: 2.655
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPei, Zen_US
dc.contributor.authorFung, PCWen_US
dc.contributor.authorCheung, RTFen_US
dc.date.accessioned2012-09-05T05:22:16Z-
dc.date.available2012-09-05T05:22:16Z-
dc.date.issued2003en_US
dc.identifier.citationJournal Of Pineal Research, 2003, v. 34 n. 2, p. 110-118en_US
dc.identifier.issn0742-3098en_US
dc.identifier.urihttp://hdl.handle.net/10722/162678-
dc.description.abstractMelatonin is a potent antioxidant and free radical scavenger. Previously, we showed that a single injection of melatonin before ischemia significantly reduced the infarct volume in both permanent and 3-hr middle cerebral artery occlusion (MCAO) rat stroke models. Nitric oxide (NO) and other free radicals play an important role in the pathogenesis of cerebral ischemia, and they have been postulated to mediate the breakdown of the blood-brain barrier (BBB) during ischemia. In this study, we evaluated the influence of melatonin, given at 30 min before MCAO, on brain NO concentration and BBB breakdown. Brain NO concentration was measured at 15 min of MCAO using electron paramagnetic resonance spectroscopy. BBB breakdown at 3 hr of reperfusion following 3 hr of MCAO was assessed using Evans blue extravasation. The relative brain NO concentration was increased to 141.69 ± 9.71% (mean ± S.E.M.; n = 9) at 15 min of MCAO. Treatment with melatonin at 1.5, 5, or 50 mg/kg significantly reduced the brain NO concentration to 104.20 ± 11.20% (n = 8), 55.67 ± 5.58% (n = 11), and 104.86 ± 12.56% (n = 9), respectively. Melatonin at 5 mg/kg did not affect Evans blue extravasation. Our results suggest that a single injection of melatonin protects against focal cerebral ischemia partly via inhibition of ischemia-induced NO production and that this regimen does not prevent BBB breakdown following ischemia-reperfusion.en_US
dc.languageengen_US
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPIen_US
dc.relation.ispartofJournal of Pineal Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood-Brain Barrieren_US
dc.subject.meshBrain Ischemia - Metabolismen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshElectron Spin Resonance Spectroscopyen_US
dc.subject.meshMaleen_US
dc.subject.meshMelatonin - Pharmacologyen_US
dc.subject.meshMiddle Cerebral Artery - Pathologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReperfusionen_US
dc.subject.meshStroke - Metabolismen_US
dc.titleMelatonin reduces nitric oxide level during ischemia but not blood-brain barrier breakdown during reperfusion in a rat middle cerebral artery occlusion stroke modelen_US
dc.typeArticleen_US
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_US
dc.identifier.authorityCheung, RTF=rp00434en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1034/j.1600-079X.2003.00014.xen_US
dc.identifier.pmid12562502-
dc.identifier.scopuseid_2-s2.0-0037373015en_US
dc.identifier.hkuros87553-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037373015&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume34en_US
dc.identifier.issue2en_US
dc.identifier.spage110en_US
dc.identifier.epage118en_US
dc.identifier.isiWOS:000180741700005-
dc.publisher.placeDenmarken_US
dc.identifier.scopusauthoridPei, Z=23051646800en_US
dc.identifier.scopusauthoridFung, PCW=7101613315en_US
dc.identifier.scopusauthoridCheung, RTF=7202397498en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats