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Article: Coenzyme Q10 protects SHSY5Y neuronal cells from beta amyloid toxicity and oxygen-glucose deprivation by inhibiting the opening of the mitochondrial permeability transition pore

TitleCoenzyme Q10 protects SHSY5Y neuronal cells from beta amyloid toxicity and oxygen-glucose deprivation by inhibiting the opening of the mitochondrial permeability transition pore
Authors
Issue Date2005
PublisherI O S Press. The Journal's web site is located at http://www.iospress.nl/html/09516433.php
Citation
Biofactors, 2005, v. 25 n. 1-4, p. 97-107 How to Cite?
AbstractCoenzyme Q10 (CoQ10) is an essential biological cofactor which increases brain mitochondrial concentration and exerts neuroprotective effects. In the present study, we exposed SHSY5Y neuroblastoma cells to neurotoxic beta amyloid peptides (Aβ) and oxygen glucose deprivation (OGD) to investigate the neuroprotective effect of 10 μM CoQ10 by measuring (i) cell viability by the MTT assay, (ii) opening of the mitochondrial permeability transition pore via the fluorescence intensity of calcein-AM, and (iii) superoxide anion concentration by hydroethidine. Cell viability (mean ± S.E.M.) was 55.5 ± 0.8% in the group exposed to Aβ + OGD, a value lower than that in the Aβ or OGD group alone (P < 0.01). CoQ10 had no neuroprotective effect on cell death induced by either Aβ or OGD, but increased cell survival in the Aβ + OGD group to 57.3 ± 1.7%, which was higher than in the group treated with vehicle (P < 0.05). The neuroprotective effect of CoQ10 was blocked by administration of 20 μM atractyloside. Pore opening and superoxide anion concentration were increased in the Aβ + OGD group relative to sham control (P < 0.01), and were attenuated to the sham level (P > 0.05) when CoQ10 was administered. Our results demonstrate that CoQ10 protects neuronal cells against Aβ neurotoxicity together with OGD by inhibiting the opening of the pore and reducing the concentration of superoxide anion. © 2005 - IOS Press and the authors. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/155331
ISSN
2015 Impact Factor: 4.504
2015 SCImago Journal Rankings: 1.683
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Gen_US
dc.contributor.authorZou, LYen_US
dc.contributor.authorCao, CMen_US
dc.contributor.authorYang, ESen_US
dc.date.accessioned2012-08-08T08:32:56Z-
dc.date.available2012-08-08T08:32:56Z-
dc.date.issued2005en_US
dc.identifier.citationBiofactors, 2005, v. 25 n. 1-4, p. 97-107en_US
dc.identifier.issn0951-6433en_US
dc.identifier.urihttp://hdl.handle.net/10722/155331-
dc.description.abstractCoenzyme Q10 (CoQ10) is an essential biological cofactor which increases brain mitochondrial concentration and exerts neuroprotective effects. In the present study, we exposed SHSY5Y neuroblastoma cells to neurotoxic beta amyloid peptides (Aβ) and oxygen glucose deprivation (OGD) to investigate the neuroprotective effect of 10 μM CoQ10 by measuring (i) cell viability by the MTT assay, (ii) opening of the mitochondrial permeability transition pore via the fluorescence intensity of calcein-AM, and (iii) superoxide anion concentration by hydroethidine. Cell viability (mean ± S.E.M.) was 55.5 ± 0.8% in the group exposed to Aβ + OGD, a value lower than that in the Aβ or OGD group alone (P < 0.01). CoQ10 had no neuroprotective effect on cell death induced by either Aβ or OGD, but increased cell survival in the Aβ + OGD group to 57.3 ± 1.7%, which was higher than in the group treated with vehicle (P < 0.05). The neuroprotective effect of CoQ10 was blocked by administration of 20 μM atractyloside. Pore opening and superoxide anion concentration were increased in the Aβ + OGD group relative to sham control (P < 0.01), and were attenuated to the sham level (P > 0.05) when CoQ10 was administered. Our results demonstrate that CoQ10 protects neuronal cells against Aβ neurotoxicity together with OGD by inhibiting the opening of the pore and reducing the concentration of superoxide anion. © 2005 - IOS Press and the authors. All rights reserved.en_US
dc.languageengen_US
dc.publisherI O S Press. The Journal's web site is located at http://www.iospress.nl/html/09516433.phpen_US
dc.relation.ispartofBioFactorsen_US
dc.subject.meshAmyloid Beta-Peptides - Toxicityen_US
dc.subject.meshAtractyloside - Pharmacologyen_US
dc.subject.meshCell Hypoxia - Physiologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshCoenzymesen_US
dc.subject.meshFluoresceins - Diagnostic Useen_US
dc.subject.meshGlucose - Deficiencyen_US
dc.subject.meshHumansen_US
dc.subject.meshLactate Dehydrogenases - Secretionen_US
dc.subject.meshMitochondrial Membrane Transport Proteins - Antagonists & Inhibitorsen_US
dc.subject.meshNeuroblastomaen_US
dc.subject.meshNeurons - Drug Effectsen_US
dc.subject.meshSuperoxides - Metabolismen_US
dc.subject.meshUbiquinone - Analogs & Derivatives - Antagonists & Inhibitors - Pharmacologyen_US
dc.titleCoenzyme Q10 protects SHSY5Y neuronal cells from beta amyloid toxicity and oxygen-glucose deprivation by inhibiting the opening of the mitochondrial permeability transition poreen_US
dc.typeArticleen_US
dc.identifier.emailYang, ES:esyang@hkueee.hku.hken_US
dc.identifier.authorityYang, ES=rp00199en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid16873934-
dc.identifier.scopuseid_2-s2.0-33746067114en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33746067114&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume25en_US
dc.identifier.issue1-4en_US
dc.identifier.spage97en_US
dc.identifier.epage107en_US
dc.identifier.isiWOS:000239639200010-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridLi, G=35767974200en_US
dc.identifier.scopusauthoridZou, LY=23391539300en_US
dc.identifier.scopusauthoridCao, CM=7401501737en_US
dc.identifier.scopusauthoridYang, ES=7202021229en_US

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