Your browser doesn't support javascript.
loading
Effects of vitamin D (VD3) supplementation on the brain mitochondrial function of male rats, in the 6-OHDA-induced model of Parkinson's disease.
Araújo de Lima, Ludmila; Oliveira Cunha, Pedro Lourenzo; Felicio Calou, Iana Bantim; Tavares Neves, Kelly Rose; Facundo, Heberty Tarso; Socorro de Barros Viana, Glauce.
Afiliação
  • Araújo de Lima L; Faculty of Medicine of the Federal University of Ceará (UFC), Brazil.
  • Oliveira Cunha PL; Faculty of Medicine of the Federal University of Cariri (UFCA), Brazil.
  • Felicio Calou IB; Federal University of Piauí (UFPI), Brazil.
  • Tavares Neves KR; Faculty of Medicine of the Federal University of Ceará (UFC), Brazil.
  • Facundo HT; Faculty of Medicine of the Federal University of Cariri (UFCA), Brazil.
  • Socorro de Barros Viana G; Faculty of Medicine of the Federal University of Ceará (UFC), Brazil. Electronic address: gbviana@live.com.
Neurochem Int ; 154: 105280, 2022 03.
Article em En | MEDLINE | ID: mdl-35026378
Mitochondria dysfunction is an important factor involved in PD pathogenesis. We reported neuroprotective actions of vitamin D (VD3) on a PD model, and now we investigated the VD3 effects on the brain mitochondrial function. We focused on oxygen consumption, respiratory control ratio (RCR), ADP/O ratio, mitochondria swelling, H2O2 production, and SOD activity. Additionally, immunohistochemistry assays for the dopamine system markers (TH and DAT) and mitochondrial markers (VDAC1 and Hsp60) were also carried out in the striata. Young adult male Wistar rats (250 g, 2.5 months age) were anesthetized and subjected to stereotaxic surgery and injection of saline (SO group) or 6-OHDA, into the right striatum. Brain mitochondria were isolated from the groups: sham-operated (SO), 6-OHDA, 6-OHDA pretreated with VD3 for 7, days before the 6-OHDA lesion (6-OHDA+VD3, pre-) or treated with VD3 for 14 days, after the 6-OHDA lesion (6-OHDA+VD3, post-). VD3 prevented decreases in oxygen consumption, RCR, and ADP/O ratio observed after 6-OHDA injury. Noteworthy, a very low (oxygen consumption and RCR) or no improvement (ADP/O) were observed in the 6-OHDA+VD3 post- group. VD3 also prevented the increased mitochondria swelling and H2O2 production and a decrease in SOD activity, respectively, in the 6-OHDA injured mitochondria. Also, VD3 supplementation protected the hemiparkinsonian brain from decreases in TH and DAT expressions and decreased the upregulation of mitochondrial markers, as VDAC 1 and Hsp60. In conclusion, VD3 showed neuroprotective actions on brain mitochondria injured by 6-OHDA and should stimulate translational studies focusing on its use as a therapeutic strategy for the treatment of neurodegenerative diseases as PD.
Assuntos
Palavras-chave
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doença de Parkinson Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Neurochem Int Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Brasil País de publicação: Reino Unido
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doença de Parkinson Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Neurochem Int Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Brasil País de publicação: Reino Unido