File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Chrysotoxine, a novel bibenzyl compound selectively antagonizes MPP +, but not rotenone, neurotoxicity in dopaminergic SH-SY5Y cells

TitleChrysotoxine, a novel bibenzyl compound selectively antagonizes MPP +, but not rotenone, neurotoxicity in dopaminergic SH-SY5Y cells
Authors
KeywordsAkt
Chrysotoxine
Mitochondrial dysfunctions
MPP +
NF-κB
Rotenone
Issue Date2012
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 2012, v. 521 n. 1, p. 76-81 How to Cite?
AbstractChrysotoxine is a naturally occurring bibenzyl compound found in medicinal Dendrobium species. We previously reported that chrysotoxine structure-specifically suppressed 6-hydroxydopamine (6-OHDA)-induced dopaminergic cell death. Whether chrysotoxine and other structurally similar bibenzyl compounds could also inhibit the neurotoxicity of 1-methyl-4-phenyl pyridinium (MPP +) and rotenone has not been investigated. We showed herein that chrysotoxine inhibited MPP +, but not rotenone, induced dopaminergic cell death in SH-SY5Y cells. The overproduction of reactive oxygen species (ROS), mitochondrial dysfunction as indexed by the decrease in membrane potential, increase in calcium concentration and NF-κB activation triggered by MPP + were blocked by chrysotoxine pretreatment. The imbalance between the pro-apoptotic signals (Bax, caspase-3, ERK and p38 MAPK) and the pro-survival signals (Akt/PI3K/GSK-3β) induced by MPP + was partially or totally rectified by chrysotoxine. The results indicated that ROS inhibition, mitochondria protection, NF-κB modulation and regulation of multiple signals determining cell survival and cell death were involved in the protective effects of chrysotoxine against MPP + toxicity in SH-SY5Y cells. Given the different toxic profiles of 6-OHDA and MPP + as compared to rotenone, our results also indicated that DAT inhibition may partially account for the neuroprotective effects of chrysotoxine. © 2012 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/159658
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSong, JXen_HK
dc.contributor.authorShaw, PCen_HK
dc.contributor.authorWong, NSen_HK
dc.contributor.authorSze, CWen_HK
dc.contributor.authorYao, XSen_HK
dc.contributor.authorTang, CWen_HK
dc.contributor.authorTong, Yen_HK
dc.contributor.authorZhang, YBen_HK
dc.date.accessioned2012-08-16T05:53:48Z-
dc.date.available2012-08-16T05:53:48Z-
dc.date.issued2012en_HK
dc.identifier.citationNeuroscience Letters, 2012, v. 521 n. 1, p. 76-81en_HK
dc.identifier.issn0304-3940en_HK
dc.identifier.urihttp://hdl.handle.net/10722/159658-
dc.description.abstractChrysotoxine is a naturally occurring bibenzyl compound found in medicinal Dendrobium species. We previously reported that chrysotoxine structure-specifically suppressed 6-hydroxydopamine (6-OHDA)-induced dopaminergic cell death. Whether chrysotoxine and other structurally similar bibenzyl compounds could also inhibit the neurotoxicity of 1-methyl-4-phenyl pyridinium (MPP +) and rotenone has not been investigated. We showed herein that chrysotoxine inhibited MPP +, but not rotenone, induced dopaminergic cell death in SH-SY5Y cells. The overproduction of reactive oxygen species (ROS), mitochondrial dysfunction as indexed by the decrease in membrane potential, increase in calcium concentration and NF-κB activation triggered by MPP + were blocked by chrysotoxine pretreatment. The imbalance between the pro-apoptotic signals (Bax, caspase-3, ERK and p38 MAPK) and the pro-survival signals (Akt/PI3K/GSK-3β) induced by MPP + was partially or totally rectified by chrysotoxine. The results indicated that ROS inhibition, mitochondria protection, NF-κB modulation and regulation of multiple signals determining cell survival and cell death were involved in the protective effects of chrysotoxine against MPP + toxicity in SH-SY5Y cells. Given the different toxic profiles of 6-OHDA and MPP + as compared to rotenone, our results also indicated that DAT inhibition may partially account for the neuroprotective effects of chrysotoxine. © 2012 Elsevier Ireland Ltd.en_HK
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_HK
dc.relation.ispartofNeuroscience Lettersen_HK
dc.subjectAkten_HK
dc.subjectChrysotoxineen_HK
dc.subjectMitochondrial dysfunctionsen_HK
dc.subjectMPP +en_HK
dc.subjectNF-κBen_HK
dc.subjectRotenoneen_HK
dc.titleChrysotoxine, a novel bibenzyl compound selectively antagonizes MPP +, but not rotenone, neurotoxicity in dopaminergic SH-SY5Y cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailSze, CW: stephens@hku.hken_HK
dc.identifier.emailTong, Y: tongyao@hku.hken_HK
dc.identifier.emailZhang, YB: ybzhang@hku.hken_HK
dc.identifier.authoritySze, CW=rp00514en_HK
dc.identifier.authorityTong, Y=rp00509en_HK
dc.identifier.authorityZhang, YB=rp01410en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neulet.2012.05.063en_HK
dc.identifier.pmid22659498-
dc.identifier.scopuseid_2-s2.0-84862607463en_HK
dc.identifier.hkuros204007en_US
dc.identifier.hkuros217965-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84862607463&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume521en_HK
dc.identifier.issue1en_HK
dc.identifier.spage76en_HK
dc.identifier.epage81en_HK
dc.identifier.isiWOS:000306448100016-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridSong, JX=24339343800en_HK
dc.identifier.scopusauthoridShaw, PC=35599523600en_HK
dc.identifier.scopusauthoridWong, NS=54790412300en_HK
dc.identifier.scopusauthoridSze, CW=23482617000en_HK
dc.identifier.scopusauthoridYao, XS=7402530417en_HK
dc.identifier.scopusauthoridTang, CW=55245633800en_HK
dc.identifier.scopusauthoridTong, Y=9045384000en_HK
dc.identifier.scopusauthoridZhang, YB=23483121900en_HK
dc.identifier.citeulike10725650-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats