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目的 研究大脑中动脉闭塞后钙调神经磷酸酶 (Calcineurin,Ca N)的活性和含量变化规律 ,探讨Ca N在脑缺血中的作用。方法 制备大鼠大脑中动脉永久性闭塞模型 ,分别测定缺血后不同时间点病灶侧大脑皮质和海马 CA1 区 Ca N的活性和含量。结果 皮质组织在缺血 6h及其后各时间点 Ca N的含量下降 ,其活性于缺血后 4h、6h和 12 h短暂性增强。海马 CA1 区 Ca N的含量于缺血后 2 4h开始降低且不恢复 ;Ca N的活性在缺血后 2 h、4h和 6h减弱 ,12 h始恢复至正常水平。可见 ,Ca N的活性与含量分离。结论 局灶脑缺血后 Ca N独特的时间变化规律显示其参与介导缺血性神经元损伤 ,可能具有毒性作用
Objective To study the changes of activity and content of calcineurin (Ca N) after occlusion of middle cerebral artery (MCA) and to explore the role of Ca N in cerebral ischemia. Methods The permanent middle cerebral artery occlusion model was established in rats. The activity and content of Ca N in focal cerebral cortex and hippocampal CA1 region at different time points after ischemia were measured respectively. Results The levels of Ca N in cortical tissue decreased at 6h and 6h after ischemia, and transiently increased at 4h, 6h and 12h after ischemia. The content of Ca N in CA1 of hippocampus began to decrease and did not recover at 24 h after ischemia. The activity of Ca N decreased at 2 h, 4 h and 6 h after ischemia and returned to the normal level at 12 h. Can be seen, Ca N activity and content separation. CONCLUSIONS: The unique Ca N changes after focal cerebral ischemia show that they may play a toxic role in mediating ischemic neuronal injury