论文部分内容阅读
目的探讨脑缺血再灌注损伤后诱导型环氧合酶(COX-2)和丙二醛(MDA)的表达及其意义,为治疗缺血性脑病提供实验依据。方法以线栓法制作大鼠大脑中动脉阻塞的局灶性脑缺血再灌注模型,采用免疫印迹法和硫代巴比妥酸法以及与神经行为相结合的方法,观测缺血再灌注侧大脑皮质内COX-2和MDA的表达和神经功能的变化,2,3,5-氯化二苯四氮唑(TTC)染色观测脑梗死体积的变化。结果MDA与COX-2的表达呈正相关(r=0.910,P<0.01)。COX-2和MDA在假手术组含量均较低,I2h/R6h两者均有明显升高,并随再灌注时间延长逐渐升高,在I2h/R24h达高峰,I2h/R48h略有下降,但仍维持在较高水平;与I2h/R24h模型组比较,川芎嗪治疗组的脑梗死体积明显减小(P<0.01),MDA含量明显降低(P<0.01)。结论脑缺血再灌注后,COX-2和MDA的表达较正常组明显增多,是导致脑缺血再灌注损伤的因素之一。川芎嗪对大鼠脑缺血再灌注损伤有保护作用。
Objective To investigate the expression of cyclooxygenase (COX-2) and malondialdehyde (MDA) after cerebral ischemia-reperfusion injury and provide experimental evidence for the treatment of ischemic encephalopathy. Methods A focal cerebral ischemia-reperfusion model of middle cerebral artery occlusion in rats was established by thread occlusion method. Western blotting, thiobarbituric acid and neurobehavioral methods were used to observe the effects of ischemia-reperfusion Changes of COX-2 and MDA expression and neurological function in cerebral cortex and changes of cerebral infarction volume with 2,3,5-chlorinated diphenyltetrazolium (TTC) staining. Results The expression of COX-2 and MDA were positively correlated (r = 0.910, P <0.01). The content of COX-2 and MDA in the sham-operation group were lower, I2h / R6h both increased significantly, and increased with the reperfusion time, reached the peak at I2h / R24h, I2h / R48h decreased slightly, Compared with I2h / R24h model group, the volume of cerebral infarction in ligustrazine-treated group decreased significantly (P <0.01) and MDA content decreased significantly (P <0.01). Conclusions The expression of COX-2 and MDA in cerebral ischemia-reperfusion rats is significantly higher than that in normal group, which is one of the factors leading to cerebral ischemia-reperfusion injury. Protective effects of ligustrazine on cerebral ischemia-reperfusion injury in rats.