摘要
目的探讨额叶细胞凋亡在慢性脑缺血所致大鼠痴呆中的作用。方法20只大鼠随机分为模型组和假手术组,模型组采用双侧颈总动脉(CCA)永久性阻断法(2-VO)建立血管性痴呆(VD)大鼠模型,假手术组仅分离暴露双侧CCA而不予结扎。采用暗回避反应法测定学习记忆能力,并应用免疫组织化学法、TUNEL法检测大鼠额叶Bcl-2蛋白表达及细胞凋亡情况。结果模型组术后1周和3周大鼠的学习记忆能力减退,潜伏期分别为(232±13)s和(220±14)s,而假手术组均为(300±0)s,2组比较差异有统计学意义(P<0.01)。模型组大鼠额叶Bcl-2的表达及凋亡细胞分别为(28.5±2.1)个/视野和(65.2±9.7)个/视野,假手术组分别为(2.6±1.0)个/视野和(4.3±1.4)个/视野,模型组较假手术组明显增高(P<0.01)。结论额叶神经细胞凋亡参与了慢性脑缺血后痴呆的发生。
Objective To explore the neural apoptosis in frontal lobe of vascular dementia rats induced by chronic cerebral ischemia. Methods Totally 20 rats were divided into model group and sham group, which underwent permanent bilateral common carotid arteries （CCA） occlusion to build vascular dementia model, while the sham group underwent sham operation without carotid artery ligation. The learning memory ability of the rats was evaluated with passive avoidance test. The expression of Bcl-2 protein and neural apoptosis in frontal lobe were determined by immunohistochemistry and TUNEL method. Results The learning memory ability of rats declined at 1 and 3 weeks after operation in model group. The latent period lasted （232± 13）s vs （220± 14）s respectively, while sham group was （300 ± 0）s （ P 〈 0.01 ）. The expression of Bel-2 protein and neural apeptosis in frontal lobe （28.5 ± 2.1 and 65.2 ± 9.7, respectively） were higher in model group than sham group, which was 2.6 - 1.0 and 4.3 ± 1.4 respectively （ P 〈 0.01 ）. Conclusion The neural apoptosis in frontal lobe may participated in the occurrence of dementia after chronic cerebral isehemia.
出处
《疑难病杂志》
CAS
2008年第11期648-650,F0003,共4页
Chinese Journal of Difficult and Complicated Cases
关键词
痴呆
血管性
细胞凋亡
额叶
大鼠
Dementia,vascular
Apoptosis,frontal lobe
Rats
