锌离子在脑缺血中作用的研究进展  

Recent progress in studies on the role of Zn^(2+) in cerebral ischemia

作　　者：李森[1] 刘克建[1] 赵咏梅[1] 

机构地区：[1]首都医科大学宣武医院神经变性病教育部重点实验室北京市老年病医疗研究中心,北京100053

出　　处：《首都医科大学学报》2013年第1期75-79,共5页Journal of Capital Medical University

基　　金：国家自然科学基金(81171242);北京市自然科学基金(7122036);省部共建国家重点实验室培育基地脑重大疾病实验室开放课题(2012NZDJ03)资助~~

摘　　要：近期研究表明,锌离子是介导脑缺血损伤的一种重要离子。缺血时,大量的锌离子从突触末端释放出来,聚集于突触后神经元内。缺血时产生的氧化应激和酸中毒也促使锌离子从胞内锌结合位点如金属硫蛋白释放。急剧的胞内锌超载可引起严重的线粒体功能障碍及活性氧簇产生,继而引起细胞坏死,而轻度的胞内锌超载则可能放大凋亡通路,导致细胞凋亡。深入研究锌离子在缺血损伤中的作用有可能为缺血性脑卒中的防治提供新策略。Recent reports have indicated that zinc ion （Zn^2＋） plays an important role in the mechanism of brain injury following cerebral ischemia. Large amount of Zn^2＋ is released from synaptic vesicles and accumulates in postsynaptic neurons following cerebral ischemia. In addition, oxidative stress and acidosis, both of which occur prominently in ischemia, can induce Zn^2＋ release from zinc-ligands such as metallothionein proteins. Intense cytosolic Zn^2＋ overloads can promote pronounced mitochondrial dysfunction and reactive oxygen species generation to trigger necrosis, whereas milder cytosolic Zn^2＋ loads may augment apoptotic pathways. Further investigation of the contribution of Zn^2＋ to the mechanism of brain injury following cerebral ischemia will likely provide new preventive and therapeutic strategies for ischemic stroke.

关 键 词：锌离子 脑缺血 脑损伤 

分 类 号：R743.31[医药卫生—神经病学与精神病学]