摘要
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, 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; TI＇C 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.
出处
《解剖学报》
CAS
CSCD
北大核心
2009年第6期886-890,共5页
Acta Anatomica Sinica
基金
山西省高校科技研究开发项目资助(200613049)
关键词
脑缺血
诱导型环氧合酶
丙二醛
川芎嗪
免疫印迹法
硫代巴比妥酸法
大鼠
Cerebral ischemic
Cyclooxygenase-2
Malonic dialdehyde
Tetramethylpyrazine
Western blotting
Barhituric acid method
Rat
