Abstract
Exercise training is a neuroprotective strategy in cerebral ischemic injury, but the underlying mechanisms are not yet clear. In the present study, we investigated the effects of treadmill exercise pretreatment on the expression of mitochondrial dynamic proteins. We examined the expression of OPA1/DLP1/MFF/Mfn1/Mfn2, which regulates mitochondrial fusion and fission, and cytochrome C oxidase subunits (COX subunits), which regulate mitochondrial functions, after middle cerebral artery occlusion (MCAO) in rats. T2-weighted magnetic resonance imaging (MRI) was evaluated as indices of brain edema after ischemia as well. Treadmill training pretreatment increased the expression levels of OPA1 and COXII/III/IV and alleviated brain edema, indicating that exercise pretreatment provided neuroprotection in cerebral ischemic injury via the regulation of mitochondrial dynamics and functions.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Western
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Brain / blood supply
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Brain / metabolism
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Brain / pathology
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Brain Ischemia / etiology
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Brain Ischemia / metabolism*
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Brain Ischemia / physiopathology
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Dynamins / metabolism
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Electron Transport Complex IV / metabolism
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GTP Phosphohydrolases / metabolism*
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Infarction, Middle Cerebral Artery / complications
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Infarction, Middle Cerebral Artery / metabolism
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Infarction, Middle Cerebral Artery / physiopathology
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Magnetic Resonance Imaging
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Male
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Membrane Proteins / metabolism
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Mitochondrial Dynamics / physiology
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Mitochondrial Proteins / metabolism*
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Physical Conditioning, Animal / physiology*
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Rats, Sprague-Dawley
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Time Factors
Substances
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Membrane Proteins
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Mfn1 protein, rat
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Mitochondrial Proteins
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Electron Transport Complex IV
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GTP Phosphohydrolases
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Mfn2 protein, rat
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Opa1 protein, rat
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Dnm1l protein, rat
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Dynamins