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[可乐定诱发的模型性癫痫发作后一氧化氮生成增加,美西多宁和α-生育酚可消除该现象]

[Model corasol-induced seizures are followed by increase of nitric oxide generation and are abolished by mexidol and alpha-tocopherol].

作者信息

Vitskova G Iu, Narkevich V B, Mikoian V D, Bashkatova V G

机构信息

Institute of Pharmacology, Russian Academy of Medical Sciences, Baltiiskaya ul. 8, Moscow, 125315 Russia.

出版信息

Eksp Klin Farmakol. 2003 Jul-Aug;66(4):3-5.

Abstract

The effect of mexidol and alpha-tocopherol on the onset and development of acute epilepsy model was studied in Wistar rats using penthylenetetrazole induced convulsions. The intensity of the nitric oxide (NO) production in the cerebral cortex was determined by a direct method using electron paramagnetic resonance. The rate of lipid peroxidation (LPO) was estimated by measuring the level of secondary products (thiobarbituric acid reactive species). The peak of penthylene-tetrazole convulsions is accompanied by a significant increase in the levels of both NO and LPO products. Mexidol (150 mg/kg) and alpha-tocopherol (100 mg/kg) hindered the development of model convulsions, prevented NO buildup, and inhibited LPO growth. It is suggested that suppression of the excess NO production in the cortex and inhibition of the LPO enhancement can be involved in the mechanism of action of antiepileptic drugs.

摘要

在Wistar大鼠中,使用戊四氮诱导惊厥,研究了美西多芬和α-生育酚对急性癫痫模型发作和发展的影响。采用电子顺磁共振直接法测定大脑皮质中一氧化氮(NO)的产生强度。通过测量次级产物(硫代巴比妥酸反应性物质)水平来评估脂质过氧化(LPO)速率。戊四氮惊厥的高峰期伴随着NO和LPO产物水平的显著增加。美西多芬(150mg/kg)和α-生育酚(100mg/kg)可抑制模型惊厥的发展,防止NO蓄积,并抑制LPO增加。提示抑制皮质中过量NO的产生和抑制LPO增强可能参与抗癫痫药物的作用机制。

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