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血管性痴呆小鼠海马CA1区锥体细胞形态结构及石杉碱甲对其影响
论文编辑部-新丝路理论网   2011-10-03 10:42:26 作者:中华医学之家:http://www.xinxi85.com 来源: 文字大小:[][][]

  摘 要 目的:观测血管性痴呆(VD)小鼠海马CA1区锥体细胞及石杉碱甲的治疗效果。方法:制作VD动物模型,并设立假手术组、石杉碱甲组;测试学习和记忆成绩;观测海马CA1区锥体细胞及顶树突,透射电镜观察其超微结构。结果:模型组学习和记忆成绩降低(P<0.05),且海马CA1区锥体细胞数目也降低(P<0.05),其顶树突总长度显著缩短,电镜下超微结构改变:细胞固缩,细胞膜及内质网膜溶解线粒体嵴减少,核膜皱缩;石杉碱甲组学习和记忆成绩均改善(P<0.05),且海马CA1区锥体细胞数目、顶树突总长度也增加(P<0.05)。结论:VD小鼠海马CA1区锥体细胞细胞数目减少、树突缩短、细胞器损害可能参与了VD的发病机制;石杉碱甲可以改善其形态结构的改变而改善临床症状。

  关键词血管性痴呆 海马 锥体细胞 透射电子显微镜 石杉碱甲

  中图分类号:R363.21;R965.1;R743.9 文献标识码:A 文章编号:1006-1533(2011)09-0443-04

  The morphology of neurons in vascular dementia

  mouse hippocampus CA1 area and the effect of huperzine*

  WANGWei-bin1,XU Cun-li1,LU Pei-yuan2

   (1. Department of Neurology,Jining No.1 Hospital,Jining,272111;

  2. Hebei Province People Hospital,Shijiazhuang,050051)

  ABSTRACTObjective: To observe the their shape and ultrastructure change in neurons in the hippocampal CA1 area of the mice with vascular dementia (VD) and the influence of drugs (huperzine) enhancing intelligence. Methods: The models of VD were established with the shamed-operation group as control group and drug groups. The changes of behavior were observed. Then,the microcosmic changes of hippocampus were observed under microscopy,neurons of CA1 section were counted comparatively and the total length of apical dendrites were measured. The ultrastructure change of hippocampal CA1 pyramidal neurons was observed under transmission electron microscopy (TEM). Results: The results of mouses learning and memory in model group were inferior (P<0.05);the results from drug group and shamed-operation group had no significant difference. The neurons in hippocampus CA1 section of model group were reduced distinctly (P<0.05),the total length of apical dendrites of hippocampal CA1 pyramidal neurons was shortened (P<0.05),but medicine group ameliorated apparently (P<0.05). Ultrastructure of hippocampus CA1 section in neurons of model group changed as follows: the multivesicular bodies and mitochondria were severely damaged,their chromatins condensated,and the perinuclear endoplasmic reticulum were damaged apparently. The ultrastructure of hippocampus CA1 section of drug group and shamed-operation group had no significant difference.Conclusion: Decrease of neurons,the shortness of the total length of apical dendrites of hippocampal CA1 pyramidal neurons,damage of multivesicular bodies and mitochondria in hippocampus CA1 section might also participate in the pathogenesis of VD,but huperzine could meliorate these changes and then alleviate the clinical symptom.

  KEY WORDSvascular dementia;hippocamppus;pyramidal neuron;transmission electron microscopy ;huperzine

  随着高龄人口和脑卒中存活率的增高,血管性痴呆(vascular dementia,VD)的发病愈来愈多。(剩余624字)

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细胞外基质金属蛋白酶诱导因子和尿激酶型纤溶酶原激活 
替米沙坦对同型半胱氨酸诱导的人脐静脉内皮细胞血管细 
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前列腺素E1对兔动脉粥样硬化易损斑块内新生血管的影 
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