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