摘要
目的研究大鼠脑缺血再灌注后凋亡相关基因Fas在海马区表达的变化,进一步探讨脑缺血再灌注后细胞凋亡的机制和GM-1的脑保护作用。方法线栓法制作大鼠局灶性脑缺血再灌注模型,同时给予GM-1治疗,采用TUNEL和免疫组化方法观察细胞凋亡及Fas蛋白在脑缺血再灌注后的变化规律。结果脑缺血再灌注后海马区神经细胞过度地表达Fas蛋白,并且该区出现明显的神经细胞凋亡;GM-1能够使Fas蛋白的表达高峰及神经细胞凋亡高峰下调。结论Fas的过度表达可能是脑缺血再灌注后神经细胞凋亡的重要原因。GM-1可能通过抑制Fas 的表达,减少神经细胞凋亡发挥脑保护作用。
Objective To study the mechanism of apoptosis after cerebral ischemia and reperfusion in rats and the role of GM-1 through observing the expression of Fas protein and apoptosis in hippocampus. Methods The focal ischemia-reperfusion model was made by thread embolisk of middle cerebral artery, and treated with GM- 1, observed the expression of Fas protein and apoptotic cell death by using in situ hybridization and terminal deoxynucleotidyl trasferase-mediated dUTP-biotininssitunickendlabeling （ TUNEL ） technique. Results Increased expression of Fas protein and increased apoptotic cells in hippocampus after cerebral ischemia and reperfusion were observed. GM-1 could decrease the expression of Fas protein and apoptotic cell death. Conclusion The increased expression of Fas protein may be the important cause of apoptotic cell death after cerebral ischemia and reperfusion. GM-1 may play a protective role by decreasing the expression of Fas protein and apoptotic cell death.
出处
《哈尔滨医科大学学报》
CAS
北大核心
2005年第4期335-336,343,共3页
Journal of Harbin Medical University
