【摘要】 目的 :研究脑缺血后不同脑温对相关基因表达的影响 ,探讨亚低温脑保护作用的机制。方法 :Sprague -Dawley(SD)大鼠 ,随机分为常温 (37- 38℃ )脑缺血、亚低温 (31- 32℃ )脑缺血、高温 (41- 4 2℃ )脑缺血和假手术组 ,每组 12只动物。脑缺血动物模型采用改良的Pulsinelli四动脉阻断法。脑组织中Fos和bcl- 2蛋白的检测采用链菌素亲生物素 -过氧化酶连接法 (SP)免疫组织化学技术。结果 :常温脑缺血再灌注可诱导Fos蛋白的表达 ,亚低温可使Fos蛋白的表达提早而增多 ,高温却使脑缺血时Fos蛋白的表达减少。常温脑缺血再灌注可诱导大脑皮质bcl- 2蛋白表达 ;亚低温增加bcl- 2蛋白表达 ;高温减少bcl- 2蛋白表达。结论 :脑缺血后即时开始亚低温可增加Fos和bcl- 2蛋白的表达 ,是亚低温脑保护作用的机制 ;脑缺血后高温则加剧脑缺血损伤更多还原

【Abstract】 Objective:To investigate the effect of brain temperature at 31-32℃,37-38℃ and 41-42℃ beginning immediately and persisting 60 min on the expression of c-fos and bcl-2 proteins in brain regions.Methods:Sprague-Dawley(SD) rats were divided into 4 groups:normothermia ischemia,mild hypothermia ischemia,hyperthermia ischermia and sham-operated group,n=12.Global cerebral ischemia was induced by modified Pulsinelli 4-vessel occlusion model.The expression of c-fos,bcl-2 proteins in brain regions were detected by Streptavidin-Speoxidase (SP) immunochemistry technique.Results:Fos protein was expressed in cerebral cortex and hippocampus after cerebral ischemia/reperfusion.In hippocampus c-fos protein expression was more rapid and strengthened in mild hypothermia group compared with normothermia group and decreased in hyperthermia group.bcl-2 proteins were expressnd in brain regions afder ischemia/reperfusion.Intraischemia mild hypothermia increased the expression of bcl-2 protein when compared with normothermia ischemia.Hyperthermia decreased the expression of bcl-2 protein when compared with the normothermia ischemia.Conclusion:Mild hypothermia beginning immediately after cerebral ischemia elevated the expression of c-fos and bcl-2 proteins ,which reduced the mortality of rats.On the contary,postischemia hyperthemia accelerated the deficit of cerebral ischemia.更多还原