大鼠脑缺血再灌注后诱导型环氧合酶和丙二醛的表达及川芎嗪的干预作用

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，I 2h/R 6h两者均有明显升高,并随再灌注时间延长逐渐升高，在I 2h/R 24h达高峰，I 2h/R 48h 略有下降，但仍维持在较高水平；与I 2h/R 24h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。

Study of the expression of cyclooxygenase-2, malonic dialdehyde and the protective effect of Tetramethylpyrazine after cerebral ischemic-reperfusion in rat

Objective To investigate the expression, relationship, significance of cyclooxygenase_2 (COX-2) and malonic dialdehyde (MDA) after cerebral ischemic-reperfusion injury and provide basis of treatment. Methods The focal cerebral ischemic-reperfusion model was established with thread embolish of middle cerebral artery. Western blotting, barhituric acid method and neurological evaluation were used to examine the expression of COX-2, MDA in cortex and the changes of neurological function;TTC staining was used to observe the changes of cerebral infarction volume. Results COX-2 prorein expression was correclated well with the MDA(r=0.910,P＜0.01). The content of COX-2 and MDA was very low in sham operation group, they were increased significantly at I2h/R6h model group, with the increase of reperfusion time,they remarkably reached its peak at I2h/R24h,they were slightly lower at I2h/R48h, but still maintained at a high level;Compared with model group, in tetramethylpyrazine(TMP) treatment group, the content of MDA and cerebral infarction volume were markedly decreased(P＜0.01). Conclusion The expression of COX-2 and MDA increases in cerebral ischemic-reperfusion injury.It indicates they may play an important role in the mechanisms of cerebral ischemic-reperfusion injury;TMP has neuroprotective effect.