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Article: Neuroprotective effects of neurokinin receptor one in dopaminergic neurons are mediated through Akt/PKB cell signaling pathway

TitleNeuroprotective effects of neurokinin receptor one in dopaminergic neurons are mediated through Akt/PKB cell signaling pathway
Authors
Issue Date2011
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharm
Citation
Neuropharmacology, 2011, v. 61 n. 8, p. 1389-1398 How to Cite?
AbstractNeurokinin one (NK1) receptor is Substance P (SP) receptor and it is abundantly distributed in the basal ganglia. Growing evidences were shown on their possible roles in the pathogenesis and treatment of Parkinson's disease (PD). NK1 receptor is a kind of G-protein-coupled-receptor (GPCR) and it links to various downstream survival signaling pathways. In the present study, treatment of NK1 receptor agonist septide [(Pyr6, Pro9)-SP (6-11)] was found to ameliorate the motor deficit in 6-hydroxydopamine (6-OHDA) lesioned rats in apomorphine rotation test. Septide treatments were also demonstrated to provide neuroprotection. In 6-OHDA lesioned rats, protection of TH immunoreactive neurons and terminals in substantia nigra (SN) and striatum was found after septide treatment. In SH-SY5Y cultures, cytotoxicity of 6-OHDA was reduced by septide pretreatment. In addition, up-regulations of phosphorylated serine-threonine kinase Akt and phosphorylated mitochondrial apoptotic protein BAD were observed in both in vivo and in vitro models, indicating the inhibition of apoptotic pathway by septide. In conclusion, septide could trigger the pro-survival Akt/PKB signaling pathway and protect dopaminergic neurons in in vivo and in vitro models against 6-OHDA toxicity. Therefore septide treatment may have therapeutic implications in treatment of PD. © 2011 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171786
ISSN
2015 Impact Factor: 4.936
2015 SCImago Journal Rankings: 2.506
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChu, JMTen_US
dc.contributor.authorChen, LWen_US
dc.contributor.authorChan, YSen_US
dc.contributor.authorYung, KKLen_US
dc.date.accessioned2012-10-30T06:17:05Z-
dc.date.available2012-10-30T06:17:05Z-
dc.date.issued2011en_US
dc.identifier.citationNeuropharmacology, 2011, v. 61 n. 8, p. 1389-1398en_US
dc.identifier.issn0028-3908en_US
dc.identifier.urihttp://hdl.handle.net/10722/171786-
dc.description.abstractNeurokinin one (NK1) receptor is Substance P (SP) receptor and it is abundantly distributed in the basal ganglia. Growing evidences were shown on their possible roles in the pathogenesis and treatment of Parkinson's disease (PD). NK1 receptor is a kind of G-protein-coupled-receptor (GPCR) and it links to various downstream survival signaling pathways. In the present study, treatment of NK1 receptor agonist septide [(Pyr6, Pro9)-SP (6-11)] was found to ameliorate the motor deficit in 6-hydroxydopamine (6-OHDA) lesioned rats in apomorphine rotation test. Septide treatments were also demonstrated to provide neuroprotection. In 6-OHDA lesioned rats, protection of TH immunoreactive neurons and terminals in substantia nigra (SN) and striatum was found after septide treatment. In SH-SY5Y cultures, cytotoxicity of 6-OHDA was reduced by septide pretreatment. In addition, up-regulations of phosphorylated serine-threonine kinase Akt and phosphorylated mitochondrial apoptotic protein BAD were observed in both in vivo and in vitro models, indicating the inhibition of apoptotic pathway by septide. In conclusion, septide could trigger the pro-survival Akt/PKB signaling pathway and protect dopaminergic neurons in in vivo and in vitro models against 6-OHDA toxicity. Therefore septide treatment may have therapeutic implications in treatment of PD. © 2011 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharmen_US
dc.relation.ispartofNeuropharmacologyen_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApomorphine - Pharmacologyen_US
dc.subject.meshCaspase 3 - Metabolismen_US
dc.subject.meshCell Death - Drug Effectsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCorpus Striatum - Drug Effects - Pathologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDopamine Agonists - Pharmacologyen_US
dc.subject.meshDopaminergic Neurons - Drug Effects - Physiologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshL-Lactate Dehydrogenase - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMotor Activityen_US
dc.subject.meshNeuroblastoma - Pathologyen_US
dc.subject.meshNeuroprotective Agents - Therapeutic Useen_US
dc.subject.meshNeurotoxicity Syndromes - Etiology - Pathology - Physiopathology - Prevention & Controlen_US
dc.subject.meshOxidopamine - Toxicityen_US
dc.subject.meshPeptide Fragments - Therapeutic Useen_US
dc.subject.meshProto-Oncogene Proteins C-Akt - Metabolismen_US
dc.subject.meshPyrrolidonecarboxylic Acid - Analogs & Derivatives - Therapeutic Useen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Neurokinin-1 - Agonists - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshRotarod Performance Testen_US
dc.subject.meshSignal Transduction - Drug Effects - Physiologyen_US
dc.subject.meshSubstance P - Analogs & Derivatives - Therapeutic Useen_US
dc.subject.meshSympatholytics - Toxicityen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTyrosine 3-Monooxygenase - Metabolismen_US
dc.subject.meshBcl-Associated Death Protein - Metabolismen_US
dc.titleNeuroprotective effects of neurokinin receptor one in dopaminergic neurons are mediated through Akt/PKB cell signaling pathwayen_US
dc.typeArticleen_US
dc.identifier.emailChan, YS:yschan@hkucc.hku.hken_US
dc.identifier.authorityChan, YS=rp00318en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.neuropharm.2011.08.027en_US
dc.identifier.pmid21907219-
dc.identifier.scopuseid_2-s2.0-80053602332en_US
dc.identifier.hkuros209191-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80053602332&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume61en_US
dc.identifier.issue8en_US
dc.identifier.spage1389en_US
dc.identifier.epage1398en_US
dc.identifier.isiWOS:000297082100025-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridChu, JMT=54079381700en_US
dc.identifier.scopusauthoridChen, LW=54079276900en_US
dc.identifier.scopusauthoridChan, YS=7403676627en_US
dc.identifier.scopusauthoridYung, KKL=13605496000en_US
dc.identifier.citeulike9776652-

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