摘要
脑出血后在血液凝固过程中释放出大量凝血酶 ,高浓度的凝血酶具有神经毒性 ,并参与脑出血后神经细胞程序性死亡。凝血酶导致神经细胞程序性死亡与其浓度、作用时间密切相关 ,可能的作用机制包括RhoA活化、PKC的过度激活、NMDA受体反应性增高等。针对凝血酶采取相应的措施 ,有可能成为防治脑出血后神经损伤的有效途径。
Generous thrombin is released during blood coagulation in intracerebral hemorrhage.Thrombin of high concentration is neurotoxic,and involved in neuro cell apoptosis in intracerebral hemorrhage.The apoptosis induced by thrombin is closely correlated to its concentration and acting time.The possible mechanism includes activation of RhoA,excessive activation of PKC,and increased reactivity of NMDA receptor.It may be a valuable way to prevent neuro injury in intracerebral hemorrhage if measures aimed directly at thrombin are taken.
出处
《医学研究生学报》
CAS
2002年第2期160-162,共3页
Journal of Medical Postgraduates
基金
重庆市卫生局"十五"重点项目 ( 2 0 0 1 2 0 0 3)
