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NBPA: a cerebral ischaemic protective agent.

J Zhang¹, X Peng, G Wei

¹Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing, China.

Clinical and Experimental Pharmacology & Physiology

|November 5, 1999

Summary

3-n-butylphthalide (NBPA), derived from celery, protects brain cells by modulating calcium currents, glutamate release, and energy metabolism. It also influences heat shock protein and c-fos mRNA expression, offering neuroprotection.

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Area of Science:

Neuroscience
Pharmacology
Biochemistry

Background:

3-n-butylphthalide (NBPA) is a derivative of 3-n-butylpathalide isolated from Apium granolens Linn.
NBPA's potential therapeutic effects, particularly in neurological conditions, warrant investigation.

Purpose of the Study:

To investigate the neuroprotective effects of NBPA.
To elucidate the mechanisms underlying NBPA's actions on cellular and molecular pathways relevant to brain injury.

Main Methods:

Electrophysiology to assess L-type calcium currents in myocardial and neuroblastoma cells.
Measurement of glutamate release from synaptosomes.
[31P] nuclear magnetic resonance spectroscopy to evaluate energy metabolism.
In situ hybridization to analyze gene expression (HSP70, c-fos).

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Assessment of nitric oxide (NO) and nitric oxide synthase (NOS) activity in a rat model of cerebral ischemia-reperfusion.

Main Results:

NBPA inhibited L-type calcium currents and glutamate release.
NBPA improved energy metabolism and modulated the expression of heat shock protein 70 mRNA and c-fos mRNA following cerebral artery occlusion.
NBPA reduced nitric oxide levels and NOS activity, and inhibited inducible NOS protein expression in a global cerebral ischemia-reperfusion model.

Conclusions:

NBPA exhibits significant neuroprotective properties.
NBPA's mechanisms of action involve the modulation of calcium channels, neurotransmitter release, cellular energy status, gene expression, and the nitric oxide pathway.
NBPA demonstrates potential as a therapeutic agent for neurological disorders involving ischemia and excitotoxicity.