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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 one of the most common diseases that are endangering human health. And the morbidity, mortality and disability rate have been increasing year by year. However, the mechanism of neurological damage after stroke remains unclear. Lack of effective treatment, looking for neuroprotective mechanisms, for the treatment of stroke is of great significance. At present, it has been found that death-associated protein kinase 1 (DAPK1) is activated as a specific signal of cell death in stroke, and is related to neuronal synaptic N-methyl-D-aspartate Binding of N-methyl-D-aspartate (NMDA) receptors triggers neuronal ischemic necrosis, which protects neurons from injury if they dissociate DAPK1 from the NMDA receptor complex A new target.