肝性脑病大鼠脑超微结构的改变
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陕西省重点领域科技创新团队项目(2012KCT-17)


Ultrastructure change of brain in rats with hepatic encephalopathy
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    摘要:

    目的 通过观察肝性脑病大鼠脑部分区域及氨对体外培养大鼠神经元超微结构的改变,讨论其病理发生机制。方法 选用健康雄性SD大鼠12只,随机分为肝性脑病模型组和正常对照组两组,每组6只。用电子透射显微镜观察硫代乙酰胺诱导的肝性脑病大鼠和体外氨中毒大鼠皮质神经元的超微结构。结果 肝性脑病大鼠神经元细胞数量减少;神经元线粒体肿胀,尼氏体数量明显减少;可见凋亡各期表现。神经胶质细胞细胞器减少,黑质的超微结构改变程度较基底核略重。体外培养氨中毒神经元变化:神经元细胞数量明显减少;细胞明显水肿,线粒体明显肿胀,尼氏体显著减少;可见不同时期的凋亡表现。结论 肝性脑病大鼠脑超微结构改变明显,其主要机制可能与氨中毒引起的神经元凋亡有关。

    Abstract:

    Objective To observe the ultrastructure change of the brain tissues in the rats with hepatic encephalopathy and determine the in vitro effect of ammonia on the ultrastructure of rat neurons in order to investigate the pathological mechanism of these changes. Methods Twelve healthy male SD rats were randomly divided into two groups: hepatic encephalopathy group and normal control group (with six in each group). Transmission electron microscopy was employed to observe the ultrastructure of the brain tissues in rats with hepatic encephalopathy induced by thioacetamide and of in vitro cultured rat neurons induced by ammonia. Results In rats with hepatic encephalopathy, the neurons were reduced in number, with swollen mitochondria, significantly decreased Nissl body quantity, and arrested in each stage of apoptosis. While, the cell organelles in glial were also decreased, and the ultrastructure changes were more serious in the nigra than in the basal nuclei. For in vitro injured rat neurons induced by ammonia, the neurons were decreased in number, with edema, swollen mitochondria, and significantly reduced Nissl body quantity, and displayed apoptosis at each stage. Conclusion Obvious changes are seen in the ultrastructure of nervous cells in rats with hepatic encephalopathy and in vitro injured neurons, which might be associated with neuron apoptosis caused by ammonia.

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李晓青*,种 莉,刘 鹏,刘 玥,唐 鹏,陈 丽,张 欣,侯 辰,李 锐,郭民侠.肝性脑病大鼠脑超微结构的改变[J].中华老年多器官疾病杂志,2014,13(08):616~620

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  • 在线发布日期: 2014-08-22
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