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

作者：Huang, Jin-zhong; Chen, Ying-zhu; Su, Min; Zheng, Hui-fen; Yang, Ya-ping; Chen, Jing; Liu, Chun-Feng^*

来源：Neuroscience Letters, 2010, 475(2): 89-94.

DOI：10.1016/j.neulet.2010.03.053

• DL-3-n-Butylphthalide
• Parkinson's disease
• Oxidative stress
• Mitochondrial membrane potential

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.

• 出版日期2010-5-14
• 单位苏州大学; 扬州大学