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

被引：123

作者：

Huang, Jin-zhong ^{[1
,3
]}

Chen, Ying-zhu ^{[3
]}

Su, Min ^{[1
]}

Zheng, Hui-fen ^{[1
]}

Yang, Ya-ping ^{[1
,2
]}

Chen, Jing ^{[1
]}

Liu, Chun-Feng ^{[1
,2
]}

机构：

[1] Soochow Univ, Affiliated Hosp 2, Dept Neurol, Suzhou 215004, Peoples R China

[2] Soochow Univ, Inst Neurosci, Lab Aging & Nervous Dis, Suzhou 215004, Peoples R China

[3] Yangzhou Univ, Clin Med Sch 1, Yangzhou 225001, Peoples R China

来源：

NEUROSCIENCE LETTERS | 2010年 / 475卷 / 02期

关键词：

DL-3-n-Butylphthalide; Parkinson's disease; Oxidative stress; Mitochondrial membrane potential; ALPHA-SYNUCLEIN; NITRIC-OXIDE; GLUTATHIONE; MPTP; NEURODEGENERATION; MECHANISMS; STRESS; ASSAY;

D O I：

10.1016/j.neulet.2010.03.053

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：89 / 94

页数：6

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