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dc.creatorTobón-Velasco, Julio César
dc.creatorVázquez-Victorio, Genaro
dc.creatorMacías-Silva, Marina
dc.creatorCuevas, Elvis
dc.creatorAli, Syed F.
dc.creatorMaldonado, Perla D.
dc.creatorGonzález-Trujano, María Eva
dc.creatorCuadrado, Antonio
dc.creatorPedraza-Chaverrí, José
dc.creatorSantamaría, Abel
dc.date.accessioned2017-06-30T03:42:13Z
dc.date.available2017-06-30T03:42:13Z
dc.date.issued2012es_ES
dc.identifier2132es_ES
dc.identifier.issn0891-5849es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/6790
dc.identifier.urihttps://doi.org/10.1016/j.freeradbiomed.2012.06.040es_ES
dc.language.isoenges_ES
dc.publisherElsevierInc.es_ES
dc.relation53 (5) 1024-1040 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleRETRACTED: S-allyl cysteine protects against 6-hydroxydopamine-induced neurotoxicity in the rat striatum: involvement of Nrf2 transcription factor activation and modulation of signaling kinase cascadeses_ES
dc.typearticlees_ES
dc.contributor.affiliationLaboratorio deAminoácidos Excitadores,Instituto Nacional de Neurología yNeurocirugía –S.S.A.,México City,Mexicoes_ES
dc.contributor.emailpedraza@unam.mxes_ES
dc.relation.jnabreviadoFREE RADIC BIOL MEDes_ES
dc.relation.journalFree radical biology and medicinees_ES
dc.identifier.placeEstados Unidoses_ES
dc.date.published2012es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1873-4596es_ES
dc.identifier.doi10.1016/j.freeradbiomed.2012.06.040es_ES
dc.description.monthSepes_ES
dc.description.abstractotrodiomaPharmacological activation at the basal ganglia of the transcription factor Nrf2, guardian of redox homeostasis, holds a strong promise for the slow progression of Parkinson's disease (PD). However, a potent Nrf2 activator in the brain still must be found. In this study, we have investigated the potential use of the antioxidant compound S-allyl cysteine (SAC) in the activation of Nrf2 in 6-hydoxydopamine (6-OHDA)-intoxicated rats. In the rat striatum, SAC by itself promoted the Nrf2 dissociation of Keap-1, its nuclear translocation, the subsequent association with small MafK protein, and further binding of the Nrf2/MafK complex to ARE sequence, as well as the up-regulation of Nrf2-dependent genes encoding the antioxidant enzymes HO-1, NQO-1, GR, and SOD-1. In vivo and in vitro experiments to identify signaling pathways activated by SAC pointed to Akt as the most likely kinase participating in Nrf2 activation by SAC. In PC12 cells, SAC stimulated the activation of Akt and ERK1/2 and inhibited JNK1/2/3 activation. In the rat striatum, the SAC-induced activation of Nrf2 is likely to contribute to inhibit the toxic effects of 6-OHDA evidenced by phase 2 antioxidant enzymes up-regulation, glutathione recovery, and attenuation of reactive oxygen species (ROS), nitric oxide (NO), and lipid peroxides formation. These early protective effects correlated with the long-term preservation of the cellular redox status, the striatal dopamine (DA) and tyrosine hydroxylase (TH) levels, and the improvement of motor skills. Therefore, this study indicates that, in addition to direct scavenging actions, the activation of Nrf2 by SAC might confer neuroprotective responses through the modulation of kinase signaling pathways in rodent models of PD, and suggests that this antioxidant molecule may have a therapeutic value in this human pathologyes_ES
dc.subject.meshmAnimalses_ES
dc.subject.meshmCysteine-Analogs & derivativeses_ES
dc.subject.meshmCysteine-Analogs & derivativeses_ES
dc.subject.meshmCysteine-Chemical synthesises_ES
dc.subject.meshmCysteine-Chemistryes_ES
dc.subject.meshmCysteine-Pharmacologyes_ES
dc.subject.meshmCysteine-Pharmacologyes_ES
dc.subject.meshmJNK Mitogen-Activated Protein Kinases-Antagonists & inhibitorses_ES
dc.subject.meshmJNK Mitogen-Activated Protein Kinases-Metabolismes_ES
dc.subject.meshmMAP Kinase Signaling System-Drug effectses_ES
dc.subject.meshmMalees_ES
dc.subject.meshmMitogen-Activated Protein Kinase 1-Metabolismes_ES
dc.subject.meshmMitogen-Activated Protein Kinase 3-Metabolismes_ES
dc.subject.meshmNF-E2-Related Factor 2-Geneticses_ES
dc.subject.meshmNF-E2-Related Factor 2-Metabolismes_ES
dc.subject.meshmNeostriatum-Drug effectses_ES
dc.subject.meshmNeostriatum-Enzymologyes_ES
dc.subject.meshmNeostriatum-Metabolismes_ES
dc.subject.meshmOxidopamine-Toxicityes_ES
dc.subject.meshmPC12 Cellses_ES
dc.subject.meshmProto-Oncogene Proteins c-akt-Metabolismes_ES
dc.subject.meshmRatses_ES
dc.subject.meshmRats, Wistares_ES
dc.subject.meshmSignal Transduction-Drug effectses_ES
dc.subject.meshmTumor Cells, Culturedes_ES
dc.subject.kwS-alil cisteína (SAC)es_ES
dc.subject.kw6-OHDAes_ES
dc.subject.kwNrf2es_ES
dc.subject.kwNeuroprotecciónes_ES
dc.subject.kwEstrés oxidativoes_ES
dc.subject.kwEnfermedad de Parkinsones_ES
dc.subject.koSACes_ES
dc.subject.ko6-OHDAes_ES
dc.subject.koNrf2es_ES
dc.subject.koNeuroprotectiones_ES
dc.subject.koOxidative stresses_ES
dc.subject.koParkinson’s diseasees_ES


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