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机构地区:[1]武汉大学医学院人体解剖学与组织胚胎学系,武汉430071
出 处:《中国组织化学与细胞化学杂志》2005年第4期370-374,共5页Chinese Journal of Histochemistry and Cytochemistry
基 金:湖北省自然科学基金资助项目(2003ABA170)
摘 要:目的探讨Aβ诱导模拟人类Alzheimer’s病(AD)大鼠模型中海马CA1区细胞色素氧化酶的表达和神经元线粒体超微结构的变化及其与老年性记忆力减退的关系,揭示Aβ对神经元的毒性机制。方法通过将Aβ25—35注射入海马建立阿尔茨海默病动物模型,使用Y形迷宫试验检测大鼠的学习记忆能力,运用酶组织化学方法测定大鼠海马CA1区细胞色素氧化酶活性,应用电镜观察大鼠海马CA1区神经细胞线粒体超微结构的变化。结果与对照组比较,接受Aβ注射的大鼠学习记忆能力降低(P<0.05),线粒体数量及形态发生了明显的变化,海马CA1区脑组织细胞的细胞色素氧化酶活性相对于对照组也有显著的下降(P<0.05)。结论Aβ在神经退行性变中的作用可能与细胞色素氧化酶表达下降及神经元线粒体超微结构的改变导致的细胞能量代谢障碍有关。Objective To study the relationship between the changes in the expression of COX and the ultrastructure of neuronal mitochondria in the hippocampus CA1 of the animal model of AD induced by β-amyloid peptide fragment 25--35, and to explore the neurotoxic mechanism of Aβ. Methods The animal model of AD was established by injecting Aβ25-35 into the hippocampus. The ability of learning and memory was tested by the performance in the Y-shape maze task. The activity of COX in the rats' hippocampal area CA1 was mensurted by the method of enzyme histochemical staining, and the ultrastructural changes of neuronal mitochondria were viewed under transmission electron microscope in hippocampal area CA1 in rats. Results The learning and memory ability of Aβ-injected rats were lower (P〈0. 05), and the number and morphology of neuronal mitochondria had distinct changes when compared with that of the controls. Furthermore, the activity of COX in hippocampal area CA1 decreased markedly in the animal model of AD than in the controls (P〈0. 05). Conclusion The role of Aβ in the process of neurodegeneration may be related to the failure of energy metabolism secondary to the inhibition of COX expression and the ultrastructural changes of neuronal mitochondria.
关 键 词:阿尔茨海默病 细胞色素氧化酶 记忆减退 Β-淀粉样多肽
分 类 号:R322.81[医药卫生—人体解剖和组织胚胎学]
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