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永久性局灶性中动脉阻断脑缺血(pMCAO)模型大鼠脑内突触相关蛋白表达的免疫组织化学观察
引用本文:刘洋,孙建宁,董世芬,刘明,张易,张硕峰.永久性局灶性中动脉阻断脑缺血(pMCAO)模型大鼠脑内突触相关蛋白表达的免疫组织化学观察[J].中国实验动物学杂志,2012(8):43-47,I0004,F0003.
作者姓名:刘洋  孙建宁  董世芬  刘明  张易  张硕峰
作者单位:[1]北京中医药大学中药学院中药药理系,北京100102 [2]贵阳中医学院,贵阳550002
摘    要:目的观察永久性局灶性中动脉阻断脑缺血(pMCAO)模型大鼠脑缺血发作后2 d、7 d脑内突触相关蛋白表达的变化。方法制作大鼠永久性局灶性中动脉阻断脑缺血(pMCAO)模型。缺血动物术后随机分为缺血2 d组、缺血7 d组,另设假手术组。在术后2 d、7 d 2个时间点采用HE染色观察动物神经病理学改变,同时采用免疫组织化学法观察动物的缺血侧脑组织突触素-I(synapsin-I)、突触后致密蛋白95(PSD-95)、α-突触核蛋白(α-synuclein)表达情况。结果与假手术组相比,缺血后,模型动物神经元大量变性坏死,数目减少,排列散乱。缺血后2 d,synapsin-I在CA1区、CA3区、皮层表达显著减少(P〈0.05或P〈0.01),PSD-95在CA1区、皮层表达显著减少(P〈0.05或P〈0.01),α-synuclein在CA1区神经元产生显著积聚(P〈0.01);缺血后7 d,synapsin-I在CA1区、皮层表达仍显著降低(P〈0.01),PSD-95在CA1区、皮层表达显著减少(P〈0.05或P〈0.01),α-synuclein在CA1、CA3、皮层表达显著增加(P〈0.05或P〈0.01)。结论 pMCAO模型大鼠在脑缺血发生后,神经突触有关蛋白的表达显著改变,并随缺血后不同时间点表达情况不同,这可能与神经元突触重塑有关。突触相关蛋白的表达与缺血损伤程度密切相关。

关 键 词:永久性局灶性中动脉阻断脑缺血模型  突触素-Ⅰ  突触后致密蛋白95  α-突触核蛋白

Immunohistochemical Observation of Brain Synaptic Proteins in the Rat Models of Permanent Middle Cerebral Artery Occlusion (pMCAO)
LIU Yang,SUN Jian-ning,DONG Shi-fen,LIU Ming,ZHANG Yi,ZHANG Shuo-feng.Immunohistochemical Observation of Brain Synaptic Proteins in the Rat Models of Permanent Middle Cerebral Artery Occlusion (pMCAO)[J].Chinese Journal of Laboratory Animal Science,2012(8):43-47,I0004,F0003.
Authors:LIU Yang  SUN Jian-ning  DONG Shi-fen  LIU Ming  ZHANG Yi  ZHANG Shuo-feng
Institution:1(1.School of Materia Medica,Beijing University of Chinese Medicine,Beijing 100102,China; 2.Guiyang College of Traditional Chinese Medicine,Guiyang 100102)
Abstract:Objective To observe synaptic protein expressions in the brain of permanent middle cerebral artery occlusion(pMCAO) model rats on 2 and 7 after ischemic attack.Methods To establish a rat model of pMCAO.The rats with ischemia were randomly divided into 2-day group and 7-day group,taking rats with no occlusion as the sham group.On d 2 and d 7 post-operation,pathological changes in ischemic brain tissue were observed with H&E staining,and expression of synapsin-I,postsynaptic density protein 95(PSD-95),α-synuclein were examined with immunohistochemical staining.Results Compared with the sham group,there were a large amount of neurons lost,and degeneration and necrosis of scattered neurons in the brain tissue in the model group.On the 2nd day post-ischemia,in the model group,expressions of synapsin-I in the CA1 and CA3 regions and cortex were significantly reduced(P〈0.05 or P〈0.01),PSD-95 in CA1 region and cortex was significantly reduced(P〈0.05 or P〈0.01),while α-synuclein in CA1 region significantly accumulated(P〈0.01).On the 7th day after ischemia,in the model group expression of synapsin-I in CA1 region and cortex were still significantly reduced(P〈0.01),PSD-95 in CA1 region and cortex also significantly reduced(P〈0.05 or P〈0.01),and α-synuclein in CA1,CA3 regions and cortex was significantly increased(P〈0.05 or P〈0.01).Conclusions In the brain tissue of pMCAO model rats,expression of synaptic proteins is significantly changed and varies along with the time-course of ischemia,probably,it might be related to synapse remodeling.The expression of synapse-associated proteins is closely related to the degree of ischemic injury.
Keywords:Permanent middle cerebral artery occlusion  pMCAO  rat model  Synapsin-I  PSD-95  a-synuclein
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