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机构地区:[1]青岛大学医学院脑血管病研究所,青岛266003
出 处:《解剖学杂志》2001年第5期411-414,共4页Chinese Journal of Anatomy
基 金:山东省自然科学基金资助项目 (Q97C0 112 5 )
摘 要:目的 :探讨大鼠局灶性脑缺血再灌注后神经细胞和血管内皮细胞凋亡的差异及其与Bcl 2和 p5 3蛋白表达的关系。方法 :应用原位末端标记技术和免疫组化方法 ,检测神经细胞和血管内细胞凋亡及Bcl 2和p5 3蛋白表达。结果 :在缺血周围区 ,缺血再灌注 2h神经细胞和内皮细胞凋亡开始增多 ,1 2~ 2 4h达高峰 ,之后逐渐减少 ,7~1 4d降至假手术组水平 ;血管内皮细胞凋亡迟于神经元凋亡 1 2~ 2 4h。Bcl 2蛋白表达于缺血再灌注 2h开始增强 ,1 2~ 2 4h达高峰 ,之后逐渐下降 ,至 7~ 1 4d接近假手术组水平。p5 3蛋白表达于缺血再灌注 6h开始增高 ,2 4~ 48h达高峰 ,之后逐渐下降 ,至 1 4d与假手术组已无显著性差异。结论 :脑缺血再灌注损伤后血管内皮细胞凋亡迟于神经元凋亡 ,Bcl 2和p5Objective:To study the differences between apoptotic neuron and endothelial cell and their relationship with the expression of Bcl 2 and p53 proteins after reperfusion of focal cerebral ischemia in rats.Methods:Coronal sections of brain were analyzed using and in situ terminal deoxynucleotdyl transferase mediated biotinylated deoxyuridine triphosphate nick end labeling and immunohistochemical staining methods to observe apoptosis and expression of Bcl 2 and p53.Results:In the ischemic penumbra,the number of apoptotic cells were increased 2 h after reperfusion,peaked at 12 24 h,then decreased successfully for 7 14d.The time of apoptotic endothelial cells was 12 24 h later than that of apoptotic neurons.The expression of Bcl 2 protein began 2 h after reperfusion,peaked at 12 24 h,and decreased for 7 14 d.P53 protein expressed 6 h after reperfusion,peaked at 24 48 h,and lasted for 14 d.Conclusion:The time of apoptotic endothelial cell is later than that of apoptotic neuron.Bcl 2 and P53 proteins play a regulatory role in the apoptotic process.
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