缺血性脑损害线粒体活性氧产生与神经兴奋性毒性的潜在联系  

Potential association between the production of reactive oxygen species in mitochondria in ischemic brain damage and neuroexcitatory toxicity

作　　者：赵云鹏 刘保林[1] 齐炼文[1] Zhao Yunpeng;Liu Baolin;Qi Lianwen(China Pharmaceutical University,Nanjing,Jiangsu 211100,China)

机构地区：[1]中国药科大学,江苏南京211100

出　　处：《医药前沿》2020年第17期6-8,共3页Journal of Frontiers of Medicine

摘　　要：缺血性脑损害主要是由于缺血再灌注初期,琥珀酸脱氢酶激活导致活性氧(Reactive oxy gen species,ROS)大量爆发。大量爆发的ROS导致神经元细胞内钙超载,进一步引起谷氨酸释放,介导神经兴奋性毒性。本文对脑损害产生的兴奋性毒性和氧化应激产生的机制进行综述,以期为药物的研究提供候选靶点。Ischemic brain damage is mainly due to the initial stage of ischemia-reperfusion,Succinic acid dehydrogenase activation leads to an explosion of Reactive oxygen species(ROS).A large number of ROS explosions lead to intracellular calcium overload in neurons,which leads to glutamate release and mediates neuroexcitotoxicity.This paper reviews the mechanism of excitatory toxicity and oxidative stress caused by brain damage,in order to provide a candidate target for drug research.

关 键 词：脑梗 活性氧 谷氨酸 钙超载 

分 类 号：R743.3[医药卫生—神经病学与精神病学]