摘要
目的 :通过系统观察大鼠全脑缺血再灌注后不同时相海马 CA1区神经元 Bcl 2、Bcl x L 及 Bax蛋白表达的改变 ,探讨该区神经元短暂脑缺血后产生选择性敏感的机制。方法 :通过四血管闭塞法建立大鼠全脑缺血再灌注模型 ,利用免疫组织化学方法观察再灌注后 1、3、5日海马 CA 1区神经元 Bcl 2、Bcl x L及 Bax蛋白表达的情况 ;并同时与海马 CA 1区神经元的病理形态学改变进行对比。结果 :全脑缺血再灌注后 1日 ,海马 CA1区 Bcl 2和 Bcl x L 蛋白呈阴性表达 ,Bax蛋白呈弱阳性表达 ;海马 CA1区神经元未见明显形态学改变。全脑缺血再灌注后 3日 ,海马 CA1区 Bcl 2和 Bcl x L 蛋白表达仍为阴性 ,而 Bax蛋白则呈明显阳性表达 ;海马 CA1区可见部分神经元死亡 ;全脑缺血再灌注后 5日 ,海马 CA1区 Bcl 2、Bcl x L 及 Bax蛋白则呈阴性表达 ;海马 CA1区神经元大部分死亡。结论 :全脑缺血再灌注后海马 CA1区神经元 Bcl 2和 Bcl x L 蛋白表达的抑制可能是其对短暂脑缺血产生选择性敏感的机制之一。
Objective:To investigate the mechanism underlying the selective vulnerability to hypoxia of neurons in hippocampal CA1 region following brain ischemia.Methods:Fourvessel occlusion was used to establish the model of global brain ischemia in rat.The expression of Bcl2,BclxL and Bax protein and the pathological changes in hippocampal CA1 region were observed on days 1,3,and 5 after brain ischemia,respectively.Results:The expression of Bcl2 and BclxL protein were negative,while the expression of the Bax protein was positive and there was no death of neuron in hippocampal CA1 region on day one following brain ischemia.The expression of Bcl2 and BclxL protein were also negative,while the expression of the Bax protein was still positive,and some neurons were dead in hippocampal CA1 region on day three following brain ischemia.On day five following brain ischemia,the expression of Bcl2,BclxL and Bax protein were negative,and the majority of the neurons in hippocampal CA1 region died.Conclusions:These findings suggested that the inhibition of the expression of Bcl2 and BclxL protein in hippocampal CA1 region after global brain ischemia may be one of the main reason for the selective vulnerability to hypoxia.
出处
《中国危重病急救医学》
CAS
CSCD
2001年第8期457-459,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金资助项目 ( No.39970 2 66)
