大鼠脑缺血后脑内MPO、NSE活性变化

Changes of myeloperoxidase and Neuron-specific enolase after middle cerebral artery occlusion in rats

目的通过测定大鼠局灶性脑缺血-再灌流后不同时点脑组织中髓过氧化物酶(MPO)和神经元特异性烯醇化酶(NSE)活性的变化,探讨炎症反应与脑缺血损伤的关系。方法用线栓法制备大鼠左侧大脑中动脉缺血-再灌流模型,检测缺血3h再灌流后6h、12h、24h、48h、72h和7d脑组织中MPO和NSE活性、脑梗死体积的变化。结果缺血组脑组织中NSE和MPO活性升高,再灌流后48h的NSE为(5.44±0.95)ng/ml,MPO为4.49±0.22;72h分别为(5.36±0.65)ng/ml和5.96±0.19,升高最为明显。脑梗死体积随再灌流时间延长而增加,第7d梗死体积百分比为(39.18±0.63)%。局灶性缺血脑组织中MPO活性与组织损伤(NSE活性)间具有高度正相关性。结论炎症反应是加重脑缺血损伤的重要因素。

Objective This study was designed to investigate the relationship between inflammation and cerebral ischemic damage. Methods The left MCA occlusion model was developed by a nylon thread which was placed within the internal carotid artery through the external carotid artery, and then was introduced into the middle cerebral artery. The activity of myeloperoxidase （MPO） and neuron specific enolase （NSE） were measured after 12h, 24h, 48h, 72h repergusion compared with the control group. The infarct size was also measured. Results The activity of MPO and NSE in the ischemia group were significantly increased especially at 48h and 72h after reperfusion. It was found that the infarct size was increasingly enlarged with the time extension after ischemia and reperfusion. There was a positive correlation between MPO and cerebral damage （NSE activity ）. Conclusions Inflammation is an important factor that aggravates the cerebral ischemic damage.