摘要
脑卒中是临床常见病、多发病,是目前危害人类健康最重要的疾病之一,且发病率、病死率、致残率呈逐年上升趋势,然而,脑卒中后神经功能损伤机制尚未明确,仍缺乏有效的治疗手段,寻找神经保护机制,对治疗脑卒中具有重要意义。目前有研究发现,脑卒中时死亡相关蛋白激酶1(death-associated protein kinase 1,DAPK1)作为一种特异性的细胞死亡信号被活化,与神经元突触外N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体结合引发神经元缺血性坏死,若将DAPK1从NMDA受体复合物上解离下来可保护神经元免受损伤,这成为治疗脑卒中的一个新靶点。
Stroke is a clinical common disease,frequently-occurring disease,which is one of the most important disease harm to human health. There is an upward trend in morbidity,mortality and disability rate. However,the damage mechanism of nerve function after stroke is not yet clear,and still lack of effective treatments. So looking for nerve protection mechanism has great significance to the treatment of stroke. Current research has found that when the stroke,the death-associated protein kinase 1（DAPK1）as a kind of specific cell death signal is activated,and combines with the synapses N-methyl-D-aspartate（NMDA）receptor causing neuronal ischemic necrosis. Separating DAPK1 from NMDA receptor complexes can protect neurons from damage,it become a new target for the treatment of stroke.
出处
《职业与健康》
CAS
2016年第9期1287-1289,1293,共4页
Occupation and Health
