局灶性脑缺血后嗜酸性神经元死亡的通路  

The pathway of eosinophilic neuronal death after focal cerebral ischemia

作　　者：王宗丽[1] 沈艳玲[1] 张元榛 付金涛 孙立元[1,2] 

机构地区：[1]桂林医学院附属医院病理科,广西桂林541004 [2]桂林医学院病理生理学教研室,广西桂林541004

出　　处：《中国医药科学》2016年第11期25-30,共6页China Medicine And Pharmacy

基　　金：国家自然科学基金(81260205);广西硕士研究生科研创新项目(YCSZ2014204)

摘　　要：目的局灶性脑缺血后产生各种类型的嗜酸性神经元(ENs)。为了探讨大鼠局灶性脑缺血后大脑皮质中心区和周边区ENs的形态学特征,及细胞死亡相关因子在ENs中的表达。方法夹闭蒙古沙鼠单侧颈总动脉制作前脑缺血模型,于3h至2周在显微镜下行ENs形态学和免疫组织化学分析。结果光镜:细胞核轻度异常的ENs缺血3h后出现于中心区,12h后出现于周边区,calcium、μ-calpain、GRP78和ubiquitin在该型ENs中呈阳性。中心区,核固缩和胞体不规则萎缩的ENs缺血12h后达峰值,calcium、μ-calpain表达进一步增高;核固缩和胞体极度萎缩的ENs 4d后达峰值,calcium、TUNEL染色呈阳性。周边区,ENs的胞体轻度萎缩,于1周后相继呈现核固缩、核碎裂、核溶解,同时calcium、TUNEL染色呈阳性。活化型caspase 3在中心区与周边区的各型ENs中均呈阴性。电镜:中心区,ENs的染色质凝集成不规则团块状,细胞质中出现大量空胞,核膜及胞膜均破裂。周边区,ENs的染色质凝集、碎裂呈不规则团块,最终均质化,核膜边界模糊,胞膜仍保持完整。结论局灶性脑缺血后ENs呈现了两种死亡途径:缺血中心区核固缩伴胞体极度萎缩;周边区核溶解伴胞体轻度萎缩。ENs不同形态学的改变与不同细胞死亡相关因子的活化相对应。Objective There were various types of eosinophilic neurons（ENs） after focal cerebral ischemia. To explore and discuss the morphological characteristics of ENs between central and peripheral areas of the cerebral cortex after focal cerebral ischemia in rats and the cell death related factors in the expression of ENs. Methods The forebrain ischemia model made of unilateral common carotid artery of clipping Mongolia gerbil was analyzed for ENs morphology and immunohistochemistry from 3h to 2 weeks under the microscope. Results Light microscopy showed that ENs ischemia with mild nuclear anomalies was in central area at 3h, and in peripheral area at 12 h, the calcium, μ-calpain, GRP78 and ubiquitin were positive in this type of ENs. In central area, the ENs ischemia of karyopyknosis and irregular cell body atrophy peaked at 12 h, the expression of calcium and μ-calpain further increased, while the ENs ischemia of karyopyknosis and cell body extreme atrophy peaked at 4d, the calcium and TUNEL staining were positive. In peripheral area, the ENs of cell body mild atrophy sequentially developed karyopyknosis, karyorrhexis and caryolysis over 1 week, at the same time, the calcium and TUNEL staining were positive. The various types＇ ENs of activated caspase3 between central and peripheral areas were negative. Electron microscropy showed that in central area, the chromatin of ENs condensed and integrated irregular mass, the chromatin had large number of empty cells, the nuclear membrane and cell membrane both ruptured, while in peripheral area, the condensation and integration of the chromatin of ENs had irregular mass, was homogenized in final, the nuclear membrane boundary was fuzzy, the cell membrane remained intact. Conclusion The ENs after focal cerebral ischemia had two death pathways. There were karyopyknosis combined with cell body extreme atrophy in ischemic central area, while there were caryolysis combines with cell body mild atrophy in peripheral area. The different morphological changes of ENs correspond

关 键 词：CALPAIN 嗜酸性神经元 前脑缺血 梗死 蒙古沙鼠 

分 类 号：R364.1[医药卫生—病理学]