环氧酶-2在大鼠局灶性脑缺血再灌注损伤中的表达及意义

目的探讨局灶性脑缺血再灌注损伤过程中环氧酶(COX)-2基因的表达及其意义。方法采用栓线法制备大鼠大脑中动脉缺血再灌注损伤模型。随机分为8组:假手术组,缺血2h组,缺血再灌注3、6、12、24、48和72h组,每组10只。评定神经功能损伤,HE染色观察脑组织形态学改变。Northern blot、Western blot和免疫组化染色方法检测脑组织的mRNA和蛋白产物表达。结果神经功能缺损表现随缺血再灌注时间的延长而逐渐加重。缺血2h组可见COX-2的mRNA和蛋白产物表达明显增加,再灌注后表达逐渐增强,再灌注12～24hCOX-2的mRNA和蛋白产物表达达到高峰。结论COX-2基因在局灶性脑缺血再灌注损伤中的表达呈动态变化过程,COX-2可能与缺血再灌注后迟发性神经细胞死亡有关。

Expression and significance COX-2 in focal ischemic reperfusion injury of middle cerebral artery in rats

Objective In order to explore the expression and significance of COX-2 during focal ischemic reperfusion injury of meddle cerebral artery in rats. Methods The model of focal ischemic reperfusion injury of middle cerebral artery was built in rats by placing an intraluminal suture. 80 rats were divided into 8 teams,which were control team,ischemia for 2 hours,ischemic reperfusion for 3 hours,6 hours,12 hours,24 hours,48 hours,and 72 hours. The nerve function was evaluated and the change of brain tissue injury was observed by HE stain. Northern blot,Western blot and immunohistochemistry were used to dectect the expression of COX-2. Result Manifestation of neurologic impairment gradually aggravated with the extension of reperfusion time. The mRNA and protein expression of COX-2 increased significantly after ischemia for 2 hours,and gradually reinforced after reperfusion,which reached the peak from 12 hours to 24 hours after reperfusion. Conclusion The expression of COX-2 gene in focal cerebral ischemia reperfusion injury was dynamic changing process. The expression of COX-2 protein may be involved in the delayed neuronal death after ischemic reperfusion injury.