Mechanisms Underlying Taurine Protection Against Glutamate-Induced Neurotoxicity
Mechanisms Underlying Taurine Protection Against Glutamate-Induced Neurotoxicity
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DOI：
10.1017/s0317167100014840
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发表时间：
2013-09
期刊：
影响因子：
--
通讯作者：
H. Ye;Hai-Bo Shi;S. Yin
中科院分区：
文献类型：
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作者：
H. Ye;Hai-Bo Shi;S. Yin
摘要：牛磺酸似乎对谷氨酸（Glu）诱导的神经元损伤具有有效的保护作用，但其潜在的分子机制尚未完全了解。可能受保护的靶点包括质膜和线粒体以及内质网（ER）膜。可通过多种作用提供保护，包括防止膜去极化、神经元兴奋性毒性和线粒体能量衰竭、细胞内游离钙（[Ca 2 +]i）增加、钙蛋白酶活化和Bcl-2水平降低。这些活动可能在牛磺酸的神经保护功能中在空间和时间上相关联。此外，发生在Glu刺激下游的事件，包括酶活性改变、细胞凋亡途径和由[Ca 2 +]i增加触发的坏死，可以被牛磺酸抑制。本文综述了牛磺酸抗谷氨酸诱导的神经元损伤的可能分子机制，为进一步研究牛磺酸的保护作用机制提供参考。
Abstract: Taurine appears to exert potent protections against glutamate (Glu)-induced injury to neurons, but the underlying molecular mechanisms are not fully understood. The possibly protected targets consist of the plasma membrane and the mitochondrial as well as endoplasmic reticulum (ER) membranes. Protection may be provided through a variety of effects, including the prevention of membrane depolarization, neuronal excitotoxicity and mitochondrial energy failure, increases in intracellular free calcium ([Ca2+]i), activation of calpain, and reduction of Bcl-2 levels. These activities are likely to be linked spatially and temporally in the neuroprotective functions of taurine. In addition, events that occur downstream of Glu stimulation, including altered enzymatic activities, apoptotic pathways, and necrosis triggered by the increased [Ca2+]i, can be inhibited by taurine. This review discusses the possible molecular mechanisms of taurine against Glu-induced neuronal injury, providing a better understanding of the protective processes, which might be helpful in the development of novel interventional strategies.