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Article: Melatonin protects SHSY5Y neuronal cells but not cultured astrocytes from ischemia due to oxygen and glucose deprivation

TitleMelatonin protects SHSY5Y neuronal cells but not cultured astrocytes from ischemia due to oxygen and glucose deprivation
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. 194-201 How to Cite?
AbstractAs a potent free radical scavenger and antioxidant, melatonin protects brain tissue against ischemia-reperfusion injury, partly via suppression of ischemia-induced production of nitric oxide, when given before ischemia-reperfusion or within 2 hr of onset of ischemia. In this study, we examined the neuroprotective effect of melatonin in an in vitro model of ischemia. Primary cultured astrocytes were subjected to 4 or 8 hr of oxygen-glucose deprivation (OGD), and cultured SHSY5Y human neuronal cells were exposed to 1 hr of OGD. Melatonin was added to the medium at the commencement of OGD to achieve different final concentrations, and cell death was quantified using the measurement of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) at 24 hr after reversion of OGD. Treatment with melatonin did not affect the astrocytic cell death following 4 or 8 hr of OGD. The relative MTT values of the neuronal cells were (as mean ± S.E.M.) 59.1 ± 2.4% in the vehicle-treated OGD group and 80.1 ± 2.7%, 82.5 ± 2.9%, 74.1 ± 2.3%, 64.2 ± 2.3%, 62.7 ± 2.8%, and 61.0 ± 3.9% in the OGD groups treated with melatonin at 10-3, 10-4, 10-5, 10-6, 10-7, and 10-8 M, respectively. Reduction in cell death was significant following treatment with melatonin at 10-3, 10-4, or 10-5 M. Reverse transcription-polymerase chain reaction showed that human mt1 and MT2 membrane receptors were not expressed in the cultured neuronal cells. Our results show that melatonin co-treatment protects cultured neuronal cells but not astrocytes against OGD-induced cell death in a dose-dependent manner and that the neuroprotection is independent of its known membrane receptors.
Persistent Identifierhttp://hdl.handle.net/10722/78365
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.accessioned2010-09-06T07:42:04Z-
dc.date.available2010-09-06T07:42:04Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Pineal Research, 2003, v. 34 n. 3, p. 194-201en_HK
dc.identifier.issn0742-3098en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78365-
dc.description.abstractAs a potent free radical scavenger and antioxidant, melatonin protects brain tissue against ischemia-reperfusion injury, partly via suppression of ischemia-induced production of nitric oxide, when given before ischemia-reperfusion or within 2 hr of onset of ischemia. In this study, we examined the neuroprotective effect of melatonin in an in vitro model of ischemia. Primary cultured astrocytes were subjected to 4 or 8 hr of oxygen-glucose deprivation (OGD), and cultured SHSY5Y human neuronal cells were exposed to 1 hr of OGD. Melatonin was added to the medium at the commencement of OGD to achieve different final concentrations, and cell death was quantified using the measurement of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) at 24 hr after reversion of OGD. Treatment with melatonin did not affect the astrocytic cell death following 4 or 8 hr of OGD. The relative MTT values of the neuronal cells were (as mean ± S.E.M.) 59.1 ± 2.4% in the vehicle-treated OGD group and 80.1 ± 2.7%, 82.5 ± 2.9%, 74.1 ± 2.3%, 64.2 ± 2.3%, 62.7 ± 2.8%, and 61.0 ± 3.9% in the OGD groups treated with melatonin at 10-3, 10-4, 10-5, 10-6, 10-7, and 10-8 M, respectively. Reduction in cell death was significant following treatment with melatonin at 10-3, 10-4, or 10-5 M. Reverse transcription-polymerase chain reaction showed that human mt1 and MT2 membrane receptors were not expressed in the cultured neuronal cells. Our results show that melatonin co-treatment protects cultured neuronal cells but not astrocytes against OGD-induced cell death in a dose-dependent manner and that the neuroprotection is independent of its known membrane receptors.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.meshAstrocytes - drug effects - pathologyen_HK
dc.subject.meshCell Death - drug effectsen_HK
dc.subject.meshCell Hypoxia - drug effectsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshGlucose - deficiencyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIschemiaen_HK
dc.subject.meshMelatonin - pharmacologyen_HK
dc.subject.meshNeurons - drug effects - pathologyen_HK
dc.subject.meshNeuroprotective Agents - pharmacologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshReceptors, Cell Surface - biosynthesisen_HK
dc.subject.meshReceptors, Cytoplasmic and Nuclear - biosynthesisen_HK
dc.subject.meshReceptors, Melatoninen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.titleMelatonin protects SHSY5Y neuronal cells but not cultured astrocytes from ischemia due to oxygen and glucose deprivationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0742-3098&volume=34&spage=194&epage=201&date=2003&atitle=Melatonin+protects+SHSY5Y+neuronal+cells+but+not+cultured+astrocytes+from+ischemia+due+to+oxygen+and+glucose+deprivationen_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.2003.00026.xen_HK
dc.identifier.pmid12614479-
dc.identifier.scopuseid_2-s2.0-0037378179en_HK
dc.identifier.hkuros87550en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037378179&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume34en_HK
dc.identifier.issue3en_HK
dc.identifier.spage194en_HK
dc.identifier.epage201en_HK
dc.identifier.isiWOS:000181331500007-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridPei, Z=23051646800en_HK
dc.identifier.scopusauthoridCheung, RTF=7202397498en_HK

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