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DL-3-n-Butylphthalide prevents oxidative damage and reduces mitochondrial dysfunction in an MPP+-induced cellular model of Parkinson's disease

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机构: [a]Department of Neurology, Second Affiliated Hospital of Soochow University, Suzhou 215004, China [b]Laboratory of Aging and Nervous Diseases, Institute of Neuroscience, Soochow University, Suzhou 215004, China [c]First Clinical Medical School of Yangzhou University, Yangzhou 225001, China
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关键词: DL-3-n-Butylphthalide Parkinson's disease Oxidative stress Mitochondrial membrane potential

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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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出版当年[2009]版:
大类 | 3 区 医学
小类 | 4 区 神经科学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 神经科学
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出版当年[2008]版:
Q3 NEUROSCIENCES
最新[2023]版:
Q3 NEUROSCIENCES

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第一作者机构: [a]Department of Neurology, Second Affiliated Hospital of Soochow University, Suzhou 215004, China [c]First Clinical Medical School of Yangzhou University, Yangzhou 225001, China
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通讯机构: [*1]Department of Neurology, Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou 215004, China
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