Neuroprotective effect of treadmill exercise possibly via regulation of lysosomal degradation molecules in mice with pharmacologically induced Parkinson's disease.
J Physiol Sci
; 68(5): 707-716, 2018 Sep.
Article
em En
| MEDLINE
| ID: mdl-29260454
ABSTRACT
Dysfunction of mitophagy, which is a selective degradation of defective mitochondria for quality control, is known to be implicated in the pathogenesis of Parkinson's disease (PD). However, how treadmill exercise (TE) regulates mitophagy-related molecules in PD remains to be elucidated. Therefore, we aimed to investigate how TE regulates α-synuclein (α-syn)-induced neurotoxicity and mitophagy-related molecules in the nigro-striatal region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mice. Our data showed that TE exhibited a significant restoration of tyrosine hydroxylase and motor coordination with suppression of α-syn expression, hallmarks of PD, possibly via up-regulation of lysosomal degradation molecules, LAMP-2 and cathepsin L, with down-regulation of p62, LC3-II/LC3-I ratio, PINK1 and parkin in the substantia nigra of MPTP mice. Therefore, these results suggest that treadmill exercise can be used as a non-invasive intervention to improve the pathological features and maintain a healthier mitochondrial network through appropriate elimination of defective mitochondria in PD.
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Base de dados:
MEDLINE
Assunto principal:
Condicionamento Físico Animal
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Transtornos Parkinsonianos
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Neuroproteção
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Lisossomos
Limite:
Animals
Idioma:
En
Revista:
J Physiol Sci
Assunto da revista:
FISIOLOGIA
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TRAUMATOLOGIA
Ano de publicação:
2018
Tipo de documento:
Article