脑缺血再灌注损伤中自由基与锌离子的相互作用

doi:10.3969/j.issn.1006-7795.2018.03.012

摘要/Abstract

摘要： 脑缺血再灌注诱导大量的自由基产生，引发氧化应激，并且引起细胞内锌离子（Zn²⁺）通过多种方式大量聚集，细胞内Zn²⁺释放和活性氧自由基（reactive oxygen species，ROS）的产生是神经元中许多毒性信号传导机制中的常见成分。已证明Zn²⁺和ROS在缺氧缺血性应激过程中积累，并在病理过程中起重要作用。释放的Zn²⁺通过多种机制诱导ROS产生，包括线粒体ROS产生，并且还通过与NADPH氧化酶相互作用等促进ROS在线粒体外的形成。Zn²⁺释放与ROS产生相互作用，最终通过影响细胞凋亡途径或信号转导导致神经元损伤。然而在特定条件下，Zn²⁺具有抗氧化作用，可保护脑损伤。因此，本文拟对自由基及Zn²⁺在脑缺血再灌注损伤中的相互作用进行综述。

关键词: 锌离子, 自由基, 氧化应激, 活性氧自由基, 脑缺血

Abstract: Cerebral ischemia/reperfusion induces the production of a large amount of free radicals, triggers oxidative stress, and results in the accumulation of intracellular zinc (Zn²⁺) in various ways. It is reported that the intracellular Zn²⁺ release and the generation of reactive oxygen species (ROS) are common ingredients in numerous toxic signaling mechanisms in neurons. Both Zn²⁺ ROS have been shown to accumulate during hypoxic-ischemic stress and play important roles in pathological processes. Liberated Zn²⁺ induces ROS generation by multiple mechanisms, including not only the induction of mitochondrial ROS production, and also the promotion of ROS formation outside the mitochondria by other routes such as interaction with NADPH oxidase. The interaction between Zn²⁺ and ROS eventually contributes to neuronal damage via apoptotic pathways or signal transduction. However, under certain conditions, Zn²⁺ has antioxidant activity and protects brain from injury. In this paper, the interaction between free radicals and Zn²⁺ following cerebral ischemia/reperfusion injury are reviewed.

Key words: Zn²⁺, free radicals, oxidative stress, reactive oxygen species, cerebral ischemia

中图分类号:

R743.3

房亚兰, 尹洁, 刘克建, 赵咏梅. 脑缺血再灌注损伤中自由基与锌离子的相互作用[J]. 首都医科大学学报, 2018, 39(3): 373-377.

Fang Yalan, Yin Jie, Liu Kejian, Zhao Yongmei. Interaction between free radicals and zinc following cerebral ischemia/reperfusion injury[J]. Journal of Capital Medical University, 2018, 39(3): 373-377.

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