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目的观察椒苯酮胺(piperphentonamine,PPTA)对大鼠脑缺血再灌注损伤后的保护作用,并探讨其作用机制。方法随机将SD大鼠分为假手术组、模型组、PPTA组(2.5,5,10 mg/kg)和阳性对照依达拉奉组(6 mg/kg)。采用大鼠大脑中动脉闭塞(MCAO)2 h再灌注模型,缺血1 h后静脉注射给药,复通灌流24 h后,采用Zea-Longa法进行神经功能缺陷评分,检测大鼠脑组织含水量,TTC染色法测定梗死体积及脑组织中SOD、MDA、GSH、NO、NOS生化指标。结果与模型组相比,PPTA组神经功能评分减低,梗死体积减少,脑组织中SOD、GSH活力增加,NOS活力降低,MDA和NO含量减少。其中以高剂量(10 mg/kg)组改变最为明显。结论 PPTA可能通过抑制脂质过氧反应和清除氧自由基等机制,发挥神经保护作用。
Objective To observe the protective effect of piperphentonamine (PPTA) on cerebral ischemia-reperfusion injury in rats and its mechanism of action. Methods SD rats were randomly divided into sham operation group, model group, PPTA group (2.5, 5, 10 mg / kg) and positive control edaravone group (6 mg / kg). The model of middle cerebral artery occlusion (MCAO) was established in rats 2 h after reperfusion. The rats were injected intravenously 1 h after ischemia and reperfusion for 24 h. The neurological deficits were evaluated by Zea-Longa method. Water volume and TTC staining to determine the infarct volume and the biochemical indexes of SOD, MDA, GSH, NO and NOS in brain tissue. Results Compared with the model group, the score of neurological function, the volume of infarction and the activity of SOD and GSH in brain tissue decreased, the activity of NOS and the content of MDA and NO in PPTA group decreased. Among them, high dose (10 mg / kg) group changes the most obvious. Conclusion PPTA may play a neuroprotective role by inhibiting lipid peroxidation and scavenging oxygen free radicals.