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肝性脑病大鼠海马齿状回神经元形态及一氧化氮合酶表达的变化
引用本文:刘冀,朱建忠,隋月林,刘锋,王晓宇,孙杨.肝性脑病大鼠海马齿状回神经元形态及一氧化氮合酶表达的变化[J].神经解剖学杂志,2012,28(3):294-300.
作者姓名:刘冀  朱建忠  隋月林  刘锋  王晓宇  孙杨
作者单位:1. 沧州医学高等专科学校,沧州,061000
2. 河北医科大学,石家庄,050017
摘    要:目的:观察肝性脑病模型组大鼠海马齿状回内神经元的变化及一氧化氮合酶(NOS)的表达,探讨海马神经元的形态学改变及一氧化氮(NO)在肝硬化和肝性脑病发病机制中的作用。方法:先对50只雄性大鼠进行Morris水迷宫测试,之后将动物分为正常对照组和实验模型组。9周后建立CCL4肝性脑病模型,分别取两组大鼠肝、海马组织进行HE染色、Nissl染色及NADPH-d染色。结果:(1)肉眼下可见模型组肝脏普遍呈坏死性肝硬化;(2)HE模型组血氨浓度明显高于正常对照组(P<0.05);(3)Nissl染色结果显示实验组大鼠海马神经元数目减少、染色较浅,胞浆内Nissl体减少或消失;(4)NADPH-d染色结果显示实验组可见粗大轴突着色,树突联系广泛;对照组则少有粗大轴突着色,树突间联系不如实验组广泛。实验组一氧化氮合酶(NOS)阳性神经元染色较对照组深,为紫蓝或深蓝色,且阳性神经元的数目较多。结论:(1)血氨增高是肝性脑病发病机制之一;(2)肝性脑病时海马受到损伤,并且一氧化氮(NO)可能介导了神经元的损伤。

关 键 词:肝性脑病  神经元  一氧化氮合酶  海马齿状回  大鼠

The morphological changes and NOS expression of neurons in dentate gyms of hippocampus in the hepatic encephalopathy rats
Liu Ji , Zhu Jianzhong , Sui Yuelin , Liu Feng , Wang Xiaoyu , Sun Yang.The morphological changes and NOS expression of neurons in dentate gyms of hippocampus in the hepatic encephalopathy rats[J].Chinese Journal of Neuroanatomy,2012,28(3):294-300.
Authors:Liu Ji  Zhu Jianzhong  Sui Yuelin  Liu Feng  Wang Xiaoyu  Sun Yang
Institution:1(1.Hebei Cangzhou Medical College,Cangzhou 061000;2.Hebei Medical University,Shijiazhuang 050017,China)
Abstract:Objective:To observe the neuronal morphological changes and the nitric oxide synthase(NOS) expression of neurons in dentate gyrus of hippocampus in the hepatic encephalopathy rat,and investigate the morphological changes of hippocampal neurons and role of nitric oxide(NO) in the pathogenesis of liver cirrhosis and hepatic encephalopathy.Methods: 50 male rats were divided into control group and experimental group,after Morris water maze test(MWM).After 9 weeks CCL4 model of hepatic encephalopathy was established,the livers and hippocampus of each groups were removed for HE,Nissl staining and histochemical staining for NADPH-d.Results:(1) Widespread necrosis of liver was detected by naked eyes in experimental group;(2) In experimental group blood ammonia was significant higher than that of control group(P<0.05);(3) Nissl staining indicated that the number of neurons in hippocampus of experimental group was less than in control group and the neurons were lightly stained with ecreased,Nissl bodies;(4) NADPH-d staining indicated that axon was stained heavily and plexus of dendrites was observed in experimental group.Fewer positive axons and dendrites were observed in control group.Compared with control groups,experimental group showed more heavily NOS-positive neurons in deep blue color and more number of positive neurons was observed.Conclusion:(1) Elevated blood ammonia is one of the reasons for hepatic encephalopathy;(2) Hepatic encephalopathy can lead to hippocampus injury,nitrogen monoxide(NO) may mediated the process.
Keywords:hepatic encephalopathy  neuron  nitric oxide synthase  hippocampus dentate gyrus  rat
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