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

Neurosci Lett. 2010 May 14;475(2):89-94. doi: 10.1016/j.neulet.2010.03.053. Epub 2010 Mar 27.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-Methyl-4-phenylpyridinium*
  • Animals
  • Antioxidants / pharmacology*
  • Apium
  • Benzofurans / pharmacology*
  • Cell Survival / drug effects
  • Cytoprotection
  • Glutathione / metabolism
  • Membrane Potential, Mitochondrial / drug effects
  • Mitochondria / drug effects*
  • Mitochondria / physiology
  • Oxidative Stress / drug effects*
  • PC12 Cells
  • Parkinson Disease, Secondary / chemically induced
  • Parkinson Disease, Secondary / metabolism*
  • Rats
  • Reactive Oxygen Species / metabolism
  • alpha-Synuclein / metabolism


  • Antioxidants
  • Benzofurans
  • Reactive Oxygen Species
  • alpha-Synuclein
  • 3-n-butylphthalide
  • Glutathione
  • 1-Methyl-4-phenylpyridinium