纳洛酮对大鼠脑缺血bcl-2和c-fos蛋白表达的影响  

Effects of naloxone on the expressions of bcl-2 and c-fos protein in rats with cerebral ischemia

作　　者：崔刚[1] 信照亮[1] 杨庆余[1] 周任[1] 屈建强[1] 

机构地区：[1]西安交通大学第二医院神经外科,陕西西安710004

出　　处：《中华神经外科疾病研究杂志》2005年第2期118-120,共3页Chinese Journal of Neurosurgical Disease Research

摘　　要：目的　探讨纳洛酮对脑缺血再灌注的神经保护机制。方法　采用线栓法制造的大鼠局灶性脑缺血再灌注模型,通过免疫组化法检测脑缺血不同再灌注时间以及经纳洛酮(5mg/kg)预处理后bcl -2和c- fos蛋白的表达。结果　脑缺血30min再灌注6h,bcl- 2和c- fos蛋白表达显著增加;再灌注24h,bcl- 2蛋白持续增高,而c- fos蛋白基本降至正常。表明纳洛酮可显著上调脑缺血后bcl -2蛋白的表达,抑制c -fos蛋白的表达。结论　纳洛酮的神经保护机制可能与其上调bcl- 2蛋白,抑制c- fos蛋白表达有关。Objective To explore the mechanism of the protective effect of naloxone on cerebral ischemia-reperfusion injury.Methods The model of focal cerebral ischemia-reperfusion injury was established in rats by suture-occluded method. The expression of bcl-2 and c-fos protein and the effect of naloxone on the expression were detected by immunohistochemical method in different periods after the ischemia-reperfusion injury.Results The expression of bcl-2 and c-fos protein increased significantly after the ischemia for 30 min followed by the reperfusion for 6 h. When the reperfusion continued for 24 h, the expression of bcl-2 increased continuously, while c-fos protein decreased to normal level. Naloxone could significantly up-regulate the expression of bcl-2 while depress the expression of c-fos protein.Conclusion The protective effect of naloxone on the cerebral ischemia-reperfusion injury is probably related to up-regulating the expression of bcl-2 and depressing the expression of c-fos protein.

关 键 词：纳洛酮 脑缺血 BCL-2 C-FOS 

分 类 号：R971[医药卫生—药品]