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。
ObjectiveTo observe the ultrastructurechangeof the brain tissues in the rats with hepatic encephalopathy and determine thein vitroeffect of ammonia on the ultrastructure of rat neurons in order to investigate the pathological mechanism of these changes.MethodsTwelve 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 ultrastructureof the brain tissuesin rats with hepatic encephalopathyinducedby thioacetamide and ofin vitro cultured rat neuronsinducedby ammonia. ResultsIn rats with hepatic encephalopathy, theneuronswere reducedinnumber,withswollen mitochondria, significantly decreasedNissl body quantity,and arrestedin each stage ofapoptosis.While, the cell organelles in glialwerealso decreased, and the ultrastructure changes were more serious in the nigra thaninthebasal nuclei.Forin vitroinjured rat neuronsinducedby ammonia, theneurons were decreased in number,withedema, swollen mitochondria,andsignificantly reducedNissl body quantity,and displayed apoptosisat each stage.Conclusion Obvious changes are seen in theultrastructure of nervouscells in rats with hepatic encephalopathyandin vitroinjured neurons, which might be associated withneuron apoptosis caused by ammonia.
出处
《中华老年多器官疾病杂志》
2014年第8期616-620,共5页
Chinese Journal of Multiple Organ Diseases in the Elderly
基金
陕西省重点领域科技创新团队项目（2012KCT-17）
关键词
肝性脑病
氨
细胞培养
超微结构
hepatic encephalopathy
ammonia
cell culture
ultrastructure
