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Article: Chrysotoxine, a novel bibenzyl compound, inhibits 6-hydroxydopamine induced apoptosis in SH-SY5Y cells via mitochondria protection and NF-κB modulation

TitleChrysotoxine, a novel bibenzyl compound, inhibits 6-hydroxydopamine induced apoptosis in SH-SY5Y cells via mitochondria protection and NF-κB modulation
Authors
Issue Date2010
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuint
Citation
Neurochemistry International, 2010, v. 57 n. 6, p. 676-689 How to Cite?
AbstractSome naturally occurring bibenzyl compounds have been reported as free radical scavengers. The present study tested our hypothesis that bibenzyl compounds may be neuroprotective against apoptosis induced by the neurotoxins. Five structurally similar bibenzyl derivatives were tested for their protective effect against 6-hydroxydopamine (6-OHDA) induced toxicity in the human neuroblastoma cell line SH-SY5Y. The results showed that one bibenzyl compound, namely chrysotoxine, significantly attenuated 6-OHDA-induced cell death. The subsequent mechanism study demonstrated that chrysotoxine significantly attenuated 6-OHDA-induced apoptosis characterized by DNA fragmentation and nuclear condensation in a dose-dependent manner. 6-OHDA-induced intracellular generation of reactive oxygen species (ROS), activation of p38 MAPK and ERK1/2, and mitochondrial dysfunctions, including the decrease of membrane potential, increase of intracellular free Ca 2+, release of cytochrome c, imbalance of Bax/Bcl-2 ratio and activation of caspase-3 were strikingly attenuated by chrysotoxine pretreatment. Meanwhile, chrysotoxine counteracted NF-κB activation by blocking its translocation to the nucleus, thereby preventing up-regulation of inducible nitric oxide synthase (iNOS) and intracellular NO release. The data provide the first evidence that chrysotoxine protects SH-SY5Y cells against 6-OHDA toxicity possibly through mitochondria protection and NF-κB modulation. Chrysotoxine is thus a candidate for further evaluation of its protection against neurodegeneration in Parkinson's disease. © 2010 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/179456
ISSN
2015 Impact Factor: 3.385
2015 SCImago Journal Rankings: 1.345
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSong, JXen_US
dc.contributor.authorShaw, PCen_US
dc.contributor.authorSze, CWen_US
dc.contributor.authorTong, Yen_US
dc.contributor.authorYao, XSen_US
dc.contributor.authorNg, TBen_US
dc.contributor.authorZhang, YBen_US
dc.date.accessioned2012-12-19T09:56:44Z-
dc.date.available2012-12-19T09:56:44Z-
dc.date.issued2010en_US
dc.identifier.citationNeurochemistry International, 2010, v. 57 n. 6, p. 676-689en_US
dc.identifier.issn0197-0186en_US
dc.identifier.urihttp://hdl.handle.net/10722/179456-
dc.description.abstractSome naturally occurring bibenzyl compounds have been reported as free radical scavengers. The present study tested our hypothesis that bibenzyl compounds may be neuroprotective against apoptosis induced by the neurotoxins. Five structurally similar bibenzyl derivatives were tested for their protective effect against 6-hydroxydopamine (6-OHDA) induced toxicity in the human neuroblastoma cell line SH-SY5Y. The results showed that one bibenzyl compound, namely chrysotoxine, significantly attenuated 6-OHDA-induced cell death. The subsequent mechanism study demonstrated that chrysotoxine significantly attenuated 6-OHDA-induced apoptosis characterized by DNA fragmentation and nuclear condensation in a dose-dependent manner. 6-OHDA-induced intracellular generation of reactive oxygen species (ROS), activation of p38 MAPK and ERK1/2, and mitochondrial dysfunctions, including the decrease of membrane potential, increase of intracellular free Ca 2+, release of cytochrome c, imbalance of Bax/Bcl-2 ratio and activation of caspase-3 were strikingly attenuated by chrysotoxine pretreatment. Meanwhile, chrysotoxine counteracted NF-κB activation by blocking its translocation to the nucleus, thereby preventing up-regulation of inducible nitric oxide synthase (iNOS) and intracellular NO release. The data provide the first evidence that chrysotoxine protects SH-SY5Y cells against 6-OHDA toxicity possibly through mitochondria protection and NF-κB modulation. Chrysotoxine is thus a candidate for further evaluation of its protection against neurodegeneration in Parkinson's disease. © 2010 Elsevier Ltd.en_US
dc.languageengen_US
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuinten_US
dc.relation.ispartofNeurochemistry Internationalen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshBibenzyls - Pharmacologyen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshDna Fragmentationen_US
dc.subject.meshHumansen_US
dc.subject.meshMitochondria - Drug Effects - Metabolismen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshOxidopamine - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshReactive Oxygen Species - Metabolismen_US
dc.titleChrysotoxine, a novel bibenzyl compound, inhibits 6-hydroxydopamine induced apoptosis in SH-SY5Y cells via mitochondria protection and NF-κB modulationen_US
dc.typeArticleen_US
dc.identifier.emailSze, CW: stephens@hku.hken_US
dc.identifier.emailTong, Y: tongyao@hku.hken_US
dc.identifier.emailZhang, YB: ybzhang@hku.hken_US
dc.identifier.authoritySze, CW=rp00514en_US
dc.identifier.authorityTong, Y=rp00509en_US
dc.identifier.authorityZhang, YB=rp01410en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.neuint.2010.08.007en_US
dc.identifier.pmid20708055-
dc.identifier.scopuseid_2-s2.0-77957021343en_US
dc.identifier.hkuros183037-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77957021343&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume57en_US
dc.identifier.issue6en_US
dc.identifier.spage676en_US
dc.identifier.epage689en_US
dc.identifier.eissn1872-9754-
dc.identifier.isiWOS:000284017000009-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridSong, JX=24339343800en_US
dc.identifier.scopusauthoridShaw, PC=35599523600en_US
dc.identifier.scopusauthoridSze, CW=23482617000en_US
dc.identifier.scopusauthoridTong, Y=9045384000en_US
dc.identifier.scopusauthoridYao, XS=7402530417en_US
dc.identifier.scopusauthoridNg, TB=35311803300en_US
dc.identifier.scopusauthoridZhang, YB=23483121900en_US
dc.identifier.citeulike7716449-

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