脑缺血再灌注后XIAP与Smac表达的实验研究

目的探讨XIAP与Smac在大鼠脑缺血再灌注损伤过程中表达水平的动态变化。方法采用Wis-tar雄性大鼠制作局灶性脑缺血再灌注模型,应用免疫组织化学方法检测脑内XIAP与Smac蛋白表达,应用尼氏染色及HE染色观察神经细胞死亡情况。结果局灶性脑缺血后半暗带区神经元内XIAP蛋白表达在再灌注后6h增高,12h表达最多,在48h趋于正常;再灌注6h胞浆中Smac免疫阳性细胞增多,24h表达最多,并且胞浆和胞核都着色,72h降至正常。结论脑缺血再灌注损伤能诱导XIAP与Smac基因表达,XIAP水平的早期增高是机体对脑损伤所作出的一种保护性反应;而Smac表达增高可能参与了神经细胞凋亡。

Experimental study on expression of XIAP and smacfollowing cerebral ischemic reperfusion injury

Objective To investigate the dynamic changes in expressioof rats.Focal cerebral ischemic reperfusion model in male Wistar rats was established.Methods Immunohistochemistry staining was used to detect the expression of XIAP and Smac.Nissel and HE stainings were used to observe the death of neuronal ceus.Results The expression of XIAP in neurous increased at 6h after the focal cerebral ischemic reperfuion injury in pemumba,and reached the highest level at 12h after reperfuion,then returned to normal 48h reperfuion.Wherease the expression of Smac increased at 6h after focal cerebral ischemic reperfuion peaking at 24h post-reperfuion,then returned to normal at 72h after reperfuion.Conclusions Cerebral ischemic reperfusion could induce the expression of XIAP and Smac.The rapid increase of XIAP expression was a protective response to the cerebral injury.However,the increased expression of Smac might be involved in neuronal apoptosis.