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作 者:罗时鹏[1] 余资江[1] 肖朝伦[1] 余彦[1] 康朝胜[1] 孙宝飞[1] 李玉美[1]
机构地区:[1]贵阳医学院基础医学院人体解剖学教研室,贵州贵阳550004
出 处:《黔南民族医专学报》2013年第1期9-13,20,共6页Journal of Qiannan Medical College for Nationalities
基 金:贵州省科技厅社会发展攻关项目(黔科合SY字[2009]3067;黔科合SY字[2012]3144号);贵州省教育厅自然科学研究项目(黔教科[2009]0139号)
摘 要:目的:初步探讨Wnt/β-catenin及相关因子在缺血再灌注小鼠海马中的表达规律。方法:将70只1月龄健康雄性昆明小鼠随机分为假手术组、缺血再灌注1 d、3 d、7 d、14 d、21 d、28d组,采用夹闭双侧颈总动脉制作小鼠缺血再灌注脑损伤模型。通过Nissl法观察海马形态结构,免疫组织化学染色方法检测Wnt/β-catenin信号通路重要信号分子β-catenin、CyclinD1的表达变化。结果:正常组海马区神经元形态及分布未见异常;缺血再灌注组随着灌注时间的增加,神经细胞排列紊乱,核固缩,核溶解,颗粒细胞呈空泡样变性,尼氏小体溶解、消失,以14 d组最为严重。正常脑组织中β-catenin、CyclinD1表达均为阴性或弱阳性;缺血再灌注组中β-catenin、CyclinD1阳性表达均显著高于正常组(P<0.05),7~14 d阳性达高峰,二者成正相关关系。结论:初步证实夹闭小鼠双侧颈总动脉的方法成功建立了脑缺血再灌注损伤的动物模型,小鼠脑缺血再灌注损伤可激发Wnt信号通路,同时增加了β-catenin、CyclinD1在海马齿状回颗粒细胞下层的表达,为进一步研究Wnt信号通路在脑缺血再灌注损伤中的作用及其机制奠定了基础。Objective: The present study aims to preliminarily discuss the expression pattern of Wnt/β-catenin and related factors in mouse hippocampus following cerebral ischemia reperfusion. Methods: 70 healthy male Kunming mice aged 1 month were randomly divided into the sham group and ischemia reperfusion 1, 3, 7, 14, 21 and 28d groups. The mouse ischemia reperfusion cerebral injury model was established by bi- lateral carotid artery occlusion. The hippocampal morphology was observed by the Nissl method and the ex- pression changes of β- catenin and CyclinD1, the important signaling molecules of Wnt/β- catenin signal pathway, were detected by immunohistochemical staining method. Results: There were no abnormality in the morphology and distribution of neurons in the hippocampus in normal group; In ischemia reperfusion group, with the increase of the perfusion time, there appeared disordered arrangement, karyopyknosis and karyolysis in nerve cells, as well as vacuolar degeneration of granular cells, nissl bodies dissolution and disappearance, most seriously in 14d group. In normal brain tissue, the expressions of β-catenin and CyclinD1 were all neg- ative or weakly positive; In ischemia reperfusion group, the positive expressions of β-catenin and CyclinD1 were all significantly higher than those in the normal group ( P 〈 0. 05 ), up to the peak during 7 ~ 14 d, with a positive correlation between them both. Conclusion It was preliminary confirmed that the animal model of cerebral ischemia reperfusion injury could be established by bilateral carotid artery occlusion and the mouse is- chemia -reperfusion injury could stimulate Wnt signaling pathway and simultaneously increase the expressionsof β- catenin t, nd CyclinD1 in the subgranular zone of the Hippoeampal dentate gyrus to lay a foundation for further research of the role and mechanism of Wnt signaling pathway in cerebral isehemia - reperfusion injury.
关 键 词:脑缺血再灌注 海马 Β-CATENIN CYCLIND1
分 类 号:R322.81[医药卫生—人体解剖和组织胚胎学]
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