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Article: The utility of melatonin in reducing cerebral damage resulting from ischemia and reperfusion

TitleThe utility of melatonin in reducing cerebral damage resulting from ischemia and reperfusion
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. 3, p. 153-160 How to Cite?
AbstractThe brain is highly susceptible to focal or global ischemia. Unless ischemia is promptly reversed, reperfusion produces further cerebral damage. Acute thrombolysis or defibrinogenation is effective only in selective patients with ischemic stroke and carries a significant risk of bleeding complications. Whereas numerous neuroprotectants were shown to be effective in experimental studies, none of them have been shown to work in clinical trials. The major pathogenetic mechanisms of ischemia/reperfusion injury include excitotoxicity, disturbed calcium ion homeostasis, overproduction of nitric oxide and other free radicals, inflammation, and apoptosis. Nitric oxide and other free radicals, the key mediators of excitotoxicity and disturbed calcium ion homeostasis, cause direct injury and also indirectly damage via inflammation and apoptosis. Melatonin is a potent free radical scavenger and an indirect antioxidant. This mini review summarizes the in vivo and in vitro evidence that melatonin protects against ischemia/reperfusion injury. There is convincing evidence from the literature that melatonin treatment is highly effective in different in vivo and in vitro models of excitotoxicity or ischemia/reperfusion in multiple animal species. Melatonin is safe and non-toxic in humans, and its administration via the oral route or intravenous injection is convenient. While more experimental studies should be conducted to further explore the neuroprotective mechanisms and to document any synergistic or additive protection from combining melatonin with thrombolysis, defibrinogenation or other neuroprotectants, interested clinical scientists should consider planning phase II and III studies to confirm the benefit of melatonin as an acute stroke treatment or a preventive measure for stroke patients.
Persistent Identifierhttp://hdl.handle.net/10722/77106
ISSN
2015 Impact Factor: 9.314
2015 SCImago Journal Rankings: 2.655
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, RTFen_HK
dc.date.accessioned2010-09-06T07:28:20Z-
dc.date.available2010-09-06T07:28:20Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Pineal Research, 2003, v. 34 n. 3, p. 153-160en_HK
dc.identifier.issn0742-3098en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77106-
dc.description.abstractThe brain is highly susceptible to focal or global ischemia. Unless ischemia is promptly reversed, reperfusion produces further cerebral damage. Acute thrombolysis or defibrinogenation is effective only in selective patients with ischemic stroke and carries a significant risk of bleeding complications. Whereas numerous neuroprotectants were shown to be effective in experimental studies, none of them have been shown to work in clinical trials. The major pathogenetic mechanisms of ischemia/reperfusion injury include excitotoxicity, disturbed calcium ion homeostasis, overproduction of nitric oxide and other free radicals, inflammation, and apoptosis. Nitric oxide and other free radicals, the key mediators of excitotoxicity and disturbed calcium ion homeostasis, cause direct injury and also indirectly damage via inflammation and apoptosis. Melatonin is a potent free radical scavenger and an indirect antioxidant. This mini review summarizes the in vivo and in vitro evidence that melatonin protects against ischemia/reperfusion injury. There is convincing evidence from the literature that melatonin treatment is highly effective in different in vivo and in vitro models of excitotoxicity or ischemia/reperfusion in multiple animal species. Melatonin is safe and non-toxic in humans, and its administration via the oral route or intravenous injection is convenient. While more experimental studies should be conducted to further explore the neuroprotective mechanisms and to document any synergistic or additive protection from combining melatonin with thrombolysis, defibrinogenation or other neuroprotectants, interested clinical scientists should consider planning phase II and III studies to confirm the benefit of melatonin as an acute stroke treatment or a preventive measure for stroke patients.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.meshHumansen_HK
dc.subject.meshMelatonin - pharmacokinetics - pharmacologyen_HK
dc.subject.meshNeurons - drug effects - pathologyen_HK
dc.subject.meshNeuroprotective Agents - pharmacologyen_HK
dc.subject.meshReperfusion Injury - drug therapy - physiopathologyen_HK
dc.titleThe utility of melatonin in reducing cerebral damage resulting from ischemia and reperfusionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0742-3098&volume=34&spage=153&epage=160&date=2003&atitle=The+utility+of+melatonin+in+reducing+cerebral+damage+resulting+from+ischemia+and+reperfusionen_HK
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_HK
dc.identifier.authorityCheung, RTF=rp00434en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1034/j.1600-079X.2003.00034.xen_HK
dc.identifier.pmid12614473-
dc.identifier.scopuseid_2-s2.0-0037378182en_HK
dc.identifier.hkuros87551en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037378182&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume34en_HK
dc.identifier.issue3en_HK
dc.identifier.spage153en_HK
dc.identifier.epage160en_HK
dc.identifier.isiWOS:000181331500001-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridCheung, RTF=7202397498en_HK

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