Journal
NEUROSCIENCE LETTERS
Volume 475, Issue 2, Pages 89-94Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2010.03.053
Keywords
DL-3-n-Butylphthalide; Parkinson's disease; Oxidative stress; Mitochondrial membrane potential
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Funding
- Suzhou Social Progress Foundation [SS0701]
- Jiangsu Province Foundation of China [07KJB320109]
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The aim of the present study was to explore the neuroprotective effects and mechanisms of action of DL-3-n-butylphthalide (NBP) in a 1-methyl-4-phenylpyridiniumion (MPP+)-induced cellular model of Parkinson's disease (PD). NBP was extracted from seeds of Apium graveolens Linn. (Chinese celery). MPP+ treatment of PC12 cells caused reduced viability, formation of reactive oxygen, and disruption of mitochondrial membrane potential. Our results indicated that NBP reduced the cytotoxicity of MPP+ by suppressing the mitochondrial permeability transition, reducing oxidative stress, and increasing the cellular GSH content. NBP also reduced the accumulation of alpha-synuclein, the main component of Lewy bodies. Given that NBP is safe and currently used in clinical trials for stroke patients, NBP will likely be a promising chemical for the treatment of PD. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
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