La maladie de Parkinson en France (serveur d'exploration)

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Moderate-Intensity Physical Exercise Protects Against Experimental 6-Hydroxydopamine-Induced Hemiparkinsonism Through Nrf2-Antioxidant Response Element Pathway.

Identifieur interne : 000197 ( PubMed/Curation ); précédent : 000196; suivant : 000198

Moderate-Intensity Physical Exercise Protects Against Experimental 6-Hydroxydopamine-Induced Hemiparkinsonism Through Nrf2-Antioxidant Response Element Pathway.

Auteurs : Aderbal Silva Aguiar [Brésil] ; Marcelo Duzzioni [Brésil] ; Aline Pertile Remor [Brésil] ; Fabrine Sales Massafera Tristão [France] ; Filipe C. Matheus [Brésil] ; Rita Raisman-Vozari [France] ; Alexandra Latini [Brésil] ; Rui Daniel Prediger [Brésil]

Source :

RBID : pubmed:26323504

English descriptors

Abstract

Exercise improves the motor symptoms of patients with Parkinson disease in a palliative manner. Existing evidence demonstrates that exercise induces neuroprotection based on the neurotrophic properties. We investigated the effect of exercise on mitochondrial physiology and oxidative stress in an animal model of hemiparkinsonism.

DOI: 10.1007/s11064-015-1709-8
PubMed: 26323504

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pubmed:26323504

Le document en format XML

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<div type="abstract" xml:lang="en">Exercise improves the motor symptoms of patients with Parkinson disease in a palliative manner. Existing evidence demonstrates that exercise induces neuroprotection based on the neurotrophic properties. We investigated the effect of exercise on mitochondrial physiology and oxidative stress in an animal model of hemiparkinsonism.</div>
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<AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Exercise improves the motor symptoms of patients with Parkinson disease in a palliative manner. Existing evidence demonstrates that exercise induces neuroprotection based on the neurotrophic properties. We investigated the effect of exercise on mitochondrial physiology and oxidative stress in an animal model of hemiparkinsonism.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">C57BL/6 mice completed a 6-week exercise program on a treadmill. We injected 6-hydroxydopamine (6-OHDA; 4 μg/2 μl) into the midstriatum. The animals progressively developed bradykinesia and R(-)-apomorphine-induced rotations that were attenuated by exercise. Transcriptional activation of protective genes is mediated by the antioxidant response element (ARE). Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) binds to ARE. We investigated the Nrf2-ARE pathway in the striatum of animals.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Exercise protected 6-OHDA-induced loss of tyrosine hydroxylase immunolabeling and activated the Nrf2-ARE pathway in the nigrostriatal pathway. Exercise stimulated mitochondrial biogenesis in the striatum of animals that was more resistant to oxidant 6-OHDA and nitric oxide donor (±)-S-nitroso-N-acetylpenicillamine.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In mice, exercise activated Nrf2-ARE signaling in the nigrostriatal pathway that was protective against the development of hemiparkinsonism.</AbstractText>
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<Keyword MajorTopicYN="N">Mitochondria</Keyword>
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<Month>11</Month>
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