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乌苏里蝮蛇神经毒素 Gln49-PLA(2)的镇痛作用机制。

Mechanisms of analgesic action of Gln49-PLA(2) from Gloydius ussurensis snake venom.

机构信息

Department of Bioscience & Biotechnology, Dalian University of Technology, Dalian 116024, People's Republic of China.

出版信息

Appl Biochem Biotechnol. 2010 Mar;160(3):773-9. doi: 10.1007/s12010-009-8573-4. Epub 2009 Mar 10.

Abstract

Gln49-PLA(2) is a phospholipase A(2) isolated from the Gloydius ussurensis snake venom. In this paper, we studied its effect on the function of neural conduction. Electrophysiological studies demonstrated that Gln49-PLA(2) reduced the amplitude of the action potential and the velocity of nerve conduction on isolated mouse sciatic nerve. Patch clamp recordings confirmed that Gln49-PLA(2) significantly decreased neural excitability by the potentiation of sodium channels and the blockade of potassium channels in nerve terminal. In freshly isolated hippocampal pyramidal neurons, 54.25% of potassium current was inhibited by 20 microg/ml Gln49-PLA(2). However, sodium current was potentiated by 158.99% under the same condition. These findings demonstrate that the effect of Gln49-PLA(2) on ion channels is the main mechanism of analgesic action.

摘要

Gln49-PLA(2) 是一种从乌苏里蝮蛇蛇毒中分离得到的磷脂酶 A(2)。本文研究了它对神经传导功能的影响。电生理学研究表明,Gln49-PLA(2) 降低了分离小鼠坐骨神经动作电位的幅度和神经传导速度。膜片钳记录证实,Gln49-PLA(2) 通过增强钠通道和阻断神经末梢钾通道,显著增加神经兴奋性。在新鲜分离的海马锥体神经元中,20μg/ml Gln49-PLA(2) 抑制 54.25%的钾电流。然而,在相同条件下,钠电流被增强 158.99%。这些发现表明,Gln49-PLA(2) 对离子通道的作用是其镇痛作用的主要机制。

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