摘要
目的:观察非竞争性NMDA受体拮抗剂美金刚对大鼠脑缺血再灌注后迟发性脑损伤的抑制作用。方法:雄性Wistar大鼠135只,随机分为假手术组、模型组及干预组,采用线栓法建立大鼠大脑中动脉闭塞(MCAO)局灶性脑缺血再灌注模型,干预组用美金刚溶液灌胃,HE染色观察神经元形态变化,免疫组织化学染色检测神经元Caspase-3的表达变化,分光光度计检测其Caspase-3、MDA含量变化。结果:再灌注后12、24和48h假手术组、模型组及干预组的Caspase-3阳性区平均积分光密度、Caspase-3酶活性和MDA含量比较,差异有统计学意义(F=63.900、246.589、437.277,41.151、82.116、106.407,387.615、209.846、475.285,P均<0.001)。干预组Caspase-3表达及MDA含量较模型组降低,而高于假手术组,差异有统计学意义(P<0.05)。结论:美金刚可下调大鼠脑缺血再灌注后Caspase-3表达及MDA含量,阻止迟发性脑损伤而发挥神经保护作用。
Aim: To investigate the inhibition of NMDA receptor antagonist memantine on the cerebral ischemic injury of delay in rats.Methods:One hundred and thirty-five male Wistar rats were randomly divided into 3 groups:sham-operation group,model group,and intervention group.The models of cerebral ischemia-reperfusion injury rats were established by the middle cerebral artery occlusion(MCAO).The rats of intervention group were treated with memantine.The changes of cell morphology and the expression of Caspase-3 in cerebral cortex neurons were observed by HE staining and immunohistochemistry technique,respectively.The contents of Caspase-3 and MDA were detected by spectrophotometer.Results:The expression of Caspase-3,Caspase-3 enzyme activity and the level of MDA among the 3 groups at 12,24,and 48 h were different(F=63.900,246.589,437.277;41.151,82.116,106.407;387.615,209.846,475.285,P0.001).The expression levels of Caspase-3 and MDA in intervention group were lower than those of model group but higher than those of sham-operation group(P〈0.05).Conclusion:NMDA receptor antagonist could suppress the expression of Caspase-3 and MDA in ischemia-reperfusion brain and inhibit injury of delay in rats to play a neuroprotective role.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2011年第5期748-751,共4页
Journal of Zhengzhou University(Medical Sciences)