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牛磺酸对抗谷氨酸诱导的神经毒性的作用机制。

Mechanisms underlying taurine protection against glutamate-induced neurotoxicity.

机构信息

Department of Otorhinolaryngology, Affiliated Sixth People's Hospital of Shanghai Jiaotong University, Shanghai, China.

出版信息

Can J Neurol Sci. 2013 Sep;40(5):628-34. doi: 10.1017/s0317167100014840.

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.

摘要

牛磺酸似乎对谷氨酸(Glu)诱导的神经元损伤具有强大的保护作用,但其中的分子机制尚不完全清楚。可能的保护靶标包括质膜和线粒体以及内质网(ER)膜。保护作用可能通过多种效应来实现,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([Ca2+]i)增加、钙蛋白酶激活以及 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,Glu 刺激后发生的事件,包括酶活性改变、凋亡途径和由[Ca2+]i 增加引发的坏死,都可以被牛磺酸抑制。本文讨论了牛磺酸对抗 Glu 诱导的神经元损伤的可能分子机制,为了解保护过程提供了更好的认识,这可能有助于开发新的干预策略。

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