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Intranasal insulin improves mitochondrial function and attenuates motor deficits in a rat 6-OHDA model of Parkinson's disease.
Iravanpour, Farideh; Dargahi, Leila; Rezaei, Mohsen; Haghani, Masoud; Heidari, Reza; Valian, Neda; Ahmadiani, Abolhassan.
Afiliación
  • Iravanpour F; Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
  • Dargahi L; Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
  • Rezaei M; Department of Toxicology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
  • Haghani M; Histomorphometry and Stereology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
  • Heidari R; Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
  • Valian N; Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
  • Ahmadiani A; Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
CNS Neurosci Ther ; 27(3): 308-319, 2021 03.
Article en En | MEDLINE | ID: mdl-33497031
AIMS: Experimental and clinical evidences demonstrate that common dysregulated pathways are involved in Parkinson's disease (PD) and type 2 diabetes. Recently, insulin treatment through intranasal (IN) approach has gained attention in PD, although the underlying mechanism of its potential therapeutic effects is still unclear. In this study, we investigated the effects of insulin treatment in a rat model of PD with emphasis on mitochondrial function indices in striatum. METHODS: Rats were treated with a daily low dose (4IU/day) of IN insulin, starting 72 h after 6-OHDA-induced lesion and continued for 14 days. Motor performance, dopaminergic cell survival, mitochondrial dehydrogenases activity, mitochondrial swelling, mitochondria permeability transition pore (mPTP), mitochondrial membrane potential (Δψm ), reactive oxygen species (ROS) formation, and glutathione (GSH) content in mitochondria, mitochondrial adenosine triphosphate (ATP), and the gene expression of PGC-1α, TFAM, Drp-1, GFAP, and Iba-1 were assessed. RESULTS: Intranasal insulin significantly reduces 6-OHDA-induced motor dysfunction and dopaminergic cell death. In parallel, it improves mitochondrial function indices and modulates mitochondria biogenesis and fission as well as activation of astrocytes and microglia. CONCLUSION: Considering the prominent role of mitochondrial dysfunction in PD pathology, IN insulin as a disease-modifying therapy for PD should be considered for extensive research.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oxidopamina / Trastornos Parkinsonianos / Trastornos Motores / Insulina / Mitocondrias Límite: Animals / Humans / Male Idioma: En Revista: CNS Neurosci Ther Asunto de la revista: NEUROLOGIA / TERAPEUTICA Año: 2021 Tipo del documento: Article País de afiliación: Irán Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oxidopamina / Trastornos Parkinsonianos / Trastornos Motores / Insulina / Mitocondrias Límite: Animals / Humans / Male Idioma: En Revista: CNS Neurosci Ther Asunto de la revista: NEUROLOGIA / TERAPEUTICA Año: 2021 Tipo del documento: Article País de afiliación: Irán Pais de publicación: Reino Unido