摘要
目的:采用全脑缺血大鼠模型研究缺血后不同时间神经细胞内Ca2+浓度的动态改变,从单细胞和分子角度探讨缺血性损伤神经元胞内Ca2+代谢的机制。方法:参照改良的Pulsinelli四血管闭塞法制备全脑缺血大鼠模型,缺血后的大鼠分别在存活2、12、24、48及72h后进行皮层神经细胞急性分离、负载荧光指示剂Fura-2/AM,用钙离子成像系统检测单个神经细胞内Ca2+的浓度。实验随机分为7组:正常组,假手术组,缺血再灌模型2h、12h、24h、48h、72h等5个时间点各一组。结果:缺血再灌注不同时点大鼠大脑皮层神经元内Ca2+浓度变化出现两次跃升:全脑缺血再灌注后2h,大鼠大脑皮层神经元内Ca2+浓度达第1次峰值,再灌12h回落至正常水平,再灌24h又升至第2次高峰,甚至远高于第1次峰值,至48h、72h又有所回落,但仍高于正常水平。结论:缺血后不同时间点神经细胞内Ca2+浓度的两次跃升与神经元缺血性损伤有关。
Objective： To study the dynamic alternation of the Ca2＋ concentration in the cortical neurons after the ischemia and reperfnsion.Methods：The global cerebral isehemie model of rats were made by the modified Pulsinelli＇ s tetra-vessel occlusion method,in which cerebral cortical neurons were acquired by acutely isolate.The Ca2＋ concentration of a single neuron was tested by the Ca2＋ image-forming system. Results：Changes of the Ca2＋ concertration of neurons with ischemia and reperfusion at different time points were examined：At 213 after reperfusion compared the sham-operated group and it was increase again with ever higher level than that of 2h time point and lasted all time course.Conclusions：The Ca2＋ concentrations in the cerebral cortical neurons of rats with global cerebral ischemia and reperfusion had two peaks at 2hand 24h time point,and elevation of intracellular Ca2＋ might be important mechanisms for neuronal damage after cortical ischemia and reperfusion.
出处
《辽宁中医药大学学报》
CAS
2008年第11期188-190,共3页
Journal of Liaoning University of Traditional Chinese Medicine
关键词
全脑缺血
不同时点
皮层神经元
Ca2+浓度
rats with ischemia and reperfusion
global cerebral cortical neurons
different time points
Ca2＋ concertration
