环氧合酶2基因在大鼠脑缺血再灌注损伤中的表达及意义

The Expression and Significance of Cyclooxygenase-2 in Ischemic Reperfusion Injury of Middle Cerebral Artery in Rats

目的探讨局灶性脑缺血再灌注损伤过程中环氧合酶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3h、6h、12h、24h、48h、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和免疫组织化学染色方法检测脑组织环氧合酶2 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组环氧合酶2 mRNA和蛋白产物表达比假手术组明显增加(P<0.01),再灌注后表达逐渐增强,再灌注12h环氧合酶2的mRNA表达达高峰(0.92±0.30),再灌注24h环氧合酶2的蛋白产物表达达高峰(0.72±0.18),与其它组比较差异有显著性(P<0.01)。结论环氧合酶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,环氧合酶2可能与缺血再灌注后迟发性神经细胞死亡有关。

Aim To explore the expression and significance of cyclooxygenase （COX-2） during the focal ischemic reperfusion injury of middle 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 groups, which were control group, ischemia for 2 hours, ischemic reperfusion for 3 hours, 6 hours, 12 hours, 24 hours, 48 hours, 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. Results 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 repeffusion, which reached the peak from 12 hours to 24 hours after reperfusion （ P 〈 0.01 ）. Conculsion The expression of COX-2 gene in focal cerebral isehemia reperfusion injury was dynamic changing process. The expression of COX-2 protein may be involved in the delayed neuronal death after ischemic reperfusion injury.