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大鼠小脑缺血再灌注损伤的细胞凋亡及尼莫通的保护作用
APOPTOSIS INDUCED BY ISCHEMIC REPERFUSION INJURY AND THE PROTECTIVE EFFECTS OF NIMOTOP ON RAT CEREBELLUM
【摘要】 采用四血管闭塞法制作全脑缺血再灌动物模型, 再灌后48 小时取小脑, 石蜡包埋切片。应用末端转移酶介导的缺口末端标记法原位检测到小脑皮质及小脑核有阳性反应的凋亡细胞, 表明细胞凋亡是迟发性神经元损伤的主要形式。缺血前30 分钟给以尼莫通能有效地减少细胞凋亡, 尼莫通对小脑缺血再灌注损伤有显著性保护作用
【Abstract】 The global cerebral ischemic rat model was established by means of occlusion of four branches of arteries. The cerebellum was obtained following 48 hours after reperfusion. The tissue was embeded in paraffin and cut as usual. The positive apoptotic neurons in both the cerebellar cortex and nucleus were observed by terminal deoxynucleotidyl transferese mediated dUTP nick ending labelling (TUNEL) in situ, demonstrating that apoptosis was the main death pattern of cell in delayed neuronal damage and Nimotop which was administrated 30 minutes before ischemic could effectively decrease the apoptosis. The result suggests that Nimotop has a signficantly protective effect against the injury induced by ischemic reperfusion on cerebellum of rats.\;
【Key words】 Ischemic reperfusion; \ Apotosis; \ Cerebellum; \ Nimotop; \ Rat;
- 【文献出处】 中国组织化学与细胞化学杂志 ,CHINESE JOURNAL OF HISTOCHEMISTRY AND CYTOCHEMISTRY , 编辑部邮箱 ,1999年03期
- 【分类号】Q26
- 【下载频次】15