Abstract
It has been confirmed that mitochondrial impairment may underlie both sporadic and familial Parkinson's disease (PD). Mitochondrial fission/fusion and biogenesis are key processes in regulating mitochondrial homeostasis. Therefore, we explored whether the protective effect of resveratrol in rotenone-induced neurotoxicity was associated with mitochondrial fission/fusion and biogenesis. The results showed that resveratrol could not only promote mitochondrial mass and DNA copy number but also improve mitochondrial homeostasis and neuron function in rats and PC12 cells damaged by rotenone. We also observed effects with alterations in proteins known to regulate mitochondrial fission/fusion and biogenesis in rotenone-induced neurotoxicity. Therefore, our findings suggest that resveratrol may prevent rotenone-induced neurotoxicity through regulating mitochondrial fission/fusion and biogenesis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / biosynthesis
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Animals
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Apoptosis / drug effects
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Cell Shape / drug effects
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Cell Survival / drug effects
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DNA, Mitochondrial / genetics
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Gene Dosage
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Male
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Mitochondria / drug effects
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Mitochondria / metabolism*
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Mitochondrial Dynamics / drug effects
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Mitochondrial Dynamics / genetics*
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Motor Activity / drug effects
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Neuroprotective Agents / pharmacology
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Neurotoxins / toxicity*
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Organelle Biogenesis*
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PC12 Cells
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
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Rats
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Rats, Sprague-Dawley
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Reactive Oxygen Species / metabolism
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Resveratrol
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Rotarod Performance Test
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Rotenone / toxicity*
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Stilbenes / pharmacology*
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Survival Analysis
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Transcription Factors / metabolism
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Transcription, Genetic / drug effects
Substances
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DNA, Mitochondrial
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Neuroprotective Agents
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Neurotoxins
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
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Ppargc1a protein, rat
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Reactive Oxygen Species
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Stilbenes
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Transcription Factors
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Rotenone
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Adenosine Triphosphate
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Resveratrol