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Article: Neuroprotective effects of ebselen are associated with the regulation of Bcl-2 and Bax proteins in cultured mouse cortical neurons

TitleNeuroprotective effects of ebselen are associated with the regulation of Bcl-2 and Bax proteins in cultured mouse cortical neurons
Authors
Issue Date2006
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 2006, v. 399 n. 3, p. 210-214 How to Cite?
AbstractThere is little information available on the mechanisms underlying the neuroprotective actions of the organoselenium compound ebselen. In this study, we sought to determine the relationship between alterations in the expression of Bcl-2 and Bax proteins and intracellular levels of calcium and the protective effects of ebselen with a concentration range of 0.01-20 μM against glutamate toxicity in cultured mouse cortical neurons. Pretreatment with ebselen at moderate doses (4-12 μM), but not at lower or higher doses, significantly improved glutamate-induced suppression of cell viability. Pretreatment with ebselen (8 μM) also prevented apoptotic alterations, completely reversed the suppression of Bcl-2 expression, and significantly inhibited Bax overexpression, but did not alter elevated intracellular concentrations of calcium induced by glutamate. Pre-, co-, and post-treatment with ebselen (8 μM) had similar potency in improving the decreased viability of glutamate-exposed cells. These results indicate that the neuroprotective effects of ebselen at low doses are associated with the regulation of Bcl-2 and Bax proteins but appear to be independent of glutamate-mediated elevation of intracellular calcium, suggesting that different mechanisms are involved in the actions of low and high dose regimens. Ebselen may be an effective agent used for early treatment of acute brain injuries. © 2006 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179433
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXu, JHen_US
dc.contributor.authorHu, HTen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorQian, YHen_US
dc.contributor.authorLiu, ZHen_US
dc.contributor.authorTan, QRen_US
dc.contributor.authorZhang, ZJen_US
dc.date.accessioned2012-12-19T09:56:27Z-
dc.date.available2012-12-19T09:56:27Z-
dc.date.issued2006en_US
dc.identifier.citationNeuroscience Letters, 2006, v. 399 n. 3, p. 210-214en_US
dc.identifier.issn0304-3940en_US
dc.identifier.urihttp://hdl.handle.net/10722/179433-
dc.description.abstractThere is little information available on the mechanisms underlying the neuroprotective actions of the organoselenium compound ebselen. In this study, we sought to determine the relationship between alterations in the expression of Bcl-2 and Bax proteins and intracellular levels of calcium and the protective effects of ebselen with a concentration range of 0.01-20 μM against glutamate toxicity in cultured mouse cortical neurons. Pretreatment with ebselen at moderate doses (4-12 μM), but not at lower or higher doses, significantly improved glutamate-induced suppression of cell viability. Pretreatment with ebselen (8 μM) also prevented apoptotic alterations, completely reversed the suppression of Bcl-2 expression, and significantly inhibited Bax overexpression, but did not alter elevated intracellular concentrations of calcium induced by glutamate. Pre-, co-, and post-treatment with ebselen (8 μM) had similar potency in improving the decreased viability of glutamate-exposed cells. These results indicate that the neuroprotective effects of ebselen at low doses are associated with the regulation of Bcl-2 and Bax proteins but appear to be independent of glutamate-mediated elevation of intracellular calcium, suggesting that different mechanisms are involved in the actions of low and high dose regimens. Ebselen may be an effective agent used for early treatment of acute brain injuries. © 2006 Elsevier Ireland Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_US
dc.relation.ispartofNeuroscience Lettersen_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshAzoles - Pharmacologyen_US
dc.subject.meshCell Count - Methodsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCerebral Cortex - Cytologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshEmbryo, Mammalianen_US
dc.subject.meshGene Expression Regulation, Developmental - Drug Effectsen_US
dc.subject.meshGlutamic Acid - Adverse Effectsen_US
dc.subject.meshMiceen_US
dc.subject.meshNeurons - Drug Effects - Metabolismen_US
dc.subject.meshNeuroprotective Agents - Pharmacologyen_US
dc.subject.meshOrganoselenium Compounds - Pharmacologyen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Metabolismen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshBcl-2-Associated X Protein - Metabolismen_US
dc.titleNeuroprotective effects of ebselen are associated with the regulation of Bcl-2 and Bax proteins in cultured mouse cortical neuronsen_US
dc.typeArticleen_US
dc.identifier.emailZhang, ZJ: zhangzj@hkucc.hku.hken_US
dc.identifier.authorityZhang, ZJ=rp01297en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.neulet.2006.02.024en_US
dc.identifier.pmid16513270-
dc.identifier.scopuseid_2-s2.0-33646152087en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646152087&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume399en_US
dc.identifier.issue3en_US
dc.identifier.spage210en_US
dc.identifier.epage214en_US
dc.identifier.isiWOS:000237839000007-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridXu, JH=16240171500en_US
dc.identifier.scopusauthoridHu, HT=35305074400en_US
dc.identifier.scopusauthoridLiu, Y=26642953800en_US
dc.identifier.scopusauthoridQian, YH=8061474000en_US
dc.identifier.scopusauthoridLiu, ZH=7406677995en_US
dc.identifier.scopusauthoridTan, QR=7102120177en_US
dc.identifier.scopusauthoridZhang, ZJ=8061473900en_US

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