Recenl reporls have indicated that zinc ion (Zn2+ ) plays an important role in the mechanism of brain injury following cerebral ischemia. Large amounl of Zn2+ is released from synaplic vesicles and accumulates in poslsynaplic neurons following cerebral ischemia. In addilion, oxidalive slress and acidosis, both of which occur prominently in ischemia, can induce Zn2+ release from zinc-ligands such as melallolhionein proteins. Intense cytosolic Zn2+ overloads can promote pronounced mitochondrial dysfunction and reactive oxygen species generation to trigger necrosis, whereas milder cytosolic Zn2+ loads may augment apoptotic pathways. Further investigation of the contribution of Zn2+ to the mechanism of brain injury following cerebral ischemia will likely provide new preventive and therapeutic strategies for ischemic stroke.%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.
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