Mechanism of Neuroprotective Function of Taurine

被引：57

作者：

Wu, Jang-Yen ^{[1
]}

Wu, Heng ^{[1
]}

Jin, Ying ^{[1
]}

Wei, Jianning ^{[1
]}

Sha, Di ^{[1
]}

Prentice, Howard ^{[1
]}

Lee, Hsin-Hsueh ^{[1
]}

Lin, Chun-Hua ^{[1
]}

Lee, Yi-Hsuan ^{[1
]}

Yang, Ling-Ling ^{[1
]}

机构：

[1] Florida Atlantic Univ, Dept Biomed Sci, Boca Raton, FL 33431 USA

来源：

TAURINE 7 | 2009年 / 643卷

关键词：

NMDA RECEPTORS; NEURONAL MIGRATION; DEATH; NEUROTRANSMITTER; OSMOREGULATION; PEROXIDATION;

D O I：

10.1007/978-0-387-75681-3_17

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Taurine has potent protective function against glutamate-induced neuronal injury presumably through its function in regulation of intracellular free calcium level, [Ca2+](i). In this communication, we report that taurine exerts its protective function through one or more of the following mechanisms: 1. Inhibition of glutamate-induced calcium influx through L-, N- and P/Q-type voltage-gated calcium channels and NMDA receptor calcium channel; 2. Attenuation of glutamate-induced membrane depolarization; 3. Prevention of glutamate-induced apoptosis via preventing glutamate-mediated down-regulation of Bcl-2; 4. Prevention of cleavage of Bcl-2 by calpain. This action of taurine is due to its inhibition on glutamate induced calpain activation. Based on these observations, we propose that taurine protects neurons against glutamate-induced neurotoxicity in part, by preventing glutamate-induced membrane depolarization, elevation of [Ca2+](i), activation of calpain, reduction of Bcl-2 and apoptosis.

引用

页码：169 / 179

页数：11

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