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NBPA: A CEREBRAL ISCHAEMIC PROTECTIVE AGENT
Author(s) -
Zhang JUNTIAN,
Peng XINQI,
Wei GUO,
Su DAN
Publication year - 1999
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.1999.03144.x
Subject(s) - nitric oxide synthase , messenger rna , chemistry , nitric oxide , ischemia , heat shock protein , glutamate receptor , medicine , pharmacology , endocrinology , microbiology and biotechnology , biochemistry , enzyme , biology , receptor , gene
SUMMARY 1. NBPA is a derivative of 3‐ n ‐butylpathalide isolated from Apium granolens Linn. 2. At concentrations ranging from 6 × 10 –6 to 10 –6 mol/L, NBPA inhibited the L‐type calcium current in guinea‐pig myocardial cells and cultured human neuroblastoma cells. 3. At 10 –6 mol/L, NBPA markedly inhibited calcium‐ dependent and ‐independent release of glutamate from synaptosomes. 4. The [ 31 P] nuclear magnetic resonance spectrum has shown that pretreatment with NBPA at 15 mg/kg, i.p., improved energy metabolism. 5. In situ hybridization has shown that 10 and 20 mg/kg, i.p., NBPA prior to cerebral artery occlusion can accelerate the expression of heat shock protein 70 mRNA and inhibit c‐fos mRNA expression. 6. It has been shown that NBPA decreases the nitric oxide content and bc nitric oxide synthase (NOS) activity in the global cerebral ischaemia–reperfusion model in rats. In addition, it has been shown that NBPA significantly inhibits the expression of inducible NOS protein.