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dc.contributor.authorClaros-Gil, Silvia 
dc.contributor.authorCabrera García, Pablo
dc.contributor.authorValverde, Nadia
dc.contributor.authorRomero Zerbo, Silvana Yanina
dc.contributor.authorLara, Estrella
dc.contributor.authorLópez-González, Manuel Víctor 
dc.contributor.authorShumilov, Kirill
dc.contributor.authorRivera-Ramírez, Alicia 
dc.contributor.authorPavía-Molina, José 
dc.contributor.authorMartin-Montañez, Elisa
dc.contributor.authorGarcía-Fernández, María Inmaculada 
dc.date.accessioned2022-07-20T06:26:53Z
dc.date.available2022-07-20T06:26:53Z
dc.date.created2022
dc.date.issued2022-07-12
dc.identifier.urihttps://hdl.handle.net/10630/24735
dc.description.abstractAims: Parkinson’s disease (PD) affects 1–3% of the population aged over 65. Stress seems to contribute to PD neuropathology, probably by dysregulation of the hypothalamic–pituitary–adrenal axis. Key factors are oxidative stress, mitochondrial dysfunction and neuronal glucocorticoid-induced toxicity. Insulin-like growth factor II (IGF-II) has shown antioxidant and neuroprotective effects in some neurodegenerative disorders. Therefore, our aim was to study IGF-II protective effects against oxidative damage on a cellular combined model of PD and mild to moderate stress, based on corticosterone (CORT) and the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP+). Methods: The dopaminergic neuronal cell line SN4741 (RRID:CVCL_S466) derived from mouse substantia nigra were exposed to 200 μM MPP+, 0.5 μM CORT or both, with or without 25 ng/mL IGF-II, for 2.5 or 6 h. Cell viability, oxidative stress parameters, mitochondrial and dopamine markers and intracellular signaling pathways were evaluated. Results: The administration of MPP+ or CORT individually led to cell damage compared to control situations, whereas the combination of both drugs produced very considerable toxic synergistic effect. IGF-II counteracts the mitochondrial-oxidative damage, protecting dopaminergic neurons from death and neurodegeneration. IGF-II promotes PKC activation and nuclear factor (erythroid-derived 2)-like 2 antioxidant response in a glucocorticoid receptor-dependent pathway, preventing oxidative cell damage and maintaining mitochondrial function. Conclusions: IGF-II capacity to protect nigral dopamine neurons against mitochondrial-oxidative damage induced by CORT and MPP+ was demonstrated. Thus, IGF-II is a potential therapeutic tool for prevention and treatment of PD patients suffering mild to moderate emotional stress.es_ES
dc.description.sponsorshipUniversidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.es_ES
dc.language.isoenges_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.subjectInsulinaes_ES
dc.subjectParkinson, Enfermedad dees_ES
dc.subject.otherParkinson’s diseasees_ES
dc.subject.otherCorticosteronees_ES
dc.subject.otherNeurotoxin 1-methyl-4-phenylpyridiniumes_ES
dc.subject.otherDopaminergic neuronses_ES
dc.subject.otherInsulin-like growth factor IIes_ES
dc.titleInsulin-like growth factor II neuroprotective effects against mitochondrial-oxidative and neuronal damage induced by CORT and MPP+ in dopaminergic neuronses_ES
dc.typeinfo:eu-repo/semantics/conferenceObjectes_ES
dc.relation.eventtitleFENS Forum 2022es_ES
dc.relation.eventplaceParíses_ES
dc.relation.eventdate09/07/2022es_ES


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