缺血后处理对大鼠脑缺血再灌注损伤后环氧合酶-2的影响  

Effects of ischemic post-conditioning on COX-2 expression in brain of rats with ischemia-reperfusion injury

作　　者：邢变枝[1] 陈晖[2] 王磊[2] 刘林[2] 

机构地区：[1]武汉大学人民医院放射科,湖北省武汉市430060 [2]武汉大学人民医院泌尿外科,湖北省武汉市430060

出　　处：《职业与健康》2013年第18期2291-2293,共3页Occupation and Health

基　　金：国家自然科学基金资助项目(项目编号:30901552;项目编号:30901494)

摘　　要：目的探讨缺血后处理对大鼠局灶性脑缺血再灌注损伤环氧合酶-2(COX-2)表达的影响,以探讨其脑保护的机制。方法成年健康SD大鼠36只,随机分为3组:假手术组(Sham),缺血再灌注损伤组(I/R),缺血后处理组(IPO)。线栓法建立大脑中动脉闭塞再灌注模型。缺血再灌注24 h后留取大脑皮质组织,免疫组化、Western blot检测COX-2蛋白的含量;逆转录聚合酶链反应(RT-PCR)方法检测COX-2 mRNA表达。结果脑缺血再灌注24 h后,脑皮质内COX-2 mRNA和COX-2蛋白的表达增加(P<0.05)。应用缺血后处理能显著地减少脑缺血再灌注后脑组织内COX-2蛋白的表达(P<0.05)。缺血再灌注24 h后,与假手术组相比,缺血再灌注损伤组和缺血后处理组COX-2 mRNA和COX-2蛋白表达明显增多(P<0.05);但与缺血再灌注损伤组相比,缺血后处理组COX-2 mRNA和COX-2蛋白表达减少(P<0.05)。结论缺血后处理能抑制大鼠脑缺血再灌注损伤皮质内COX-2的表达,这可能是其脑保护作用的部分机制。[ Objective ] To investigate the protective effect of ischemic post-conditioning on COX-2 expression in cerebral ischemia reperfusion injury （I/R）, and to discuss its protective mechanisms. [ Methods] A total of 36 healthy adult SD rats were randomly divided into 3 groups ： sham group, I/R group and IPO group. SD rat model of focal ischemic reperfusion was induced by intraluminal middle cerebral artery occlusion （ MCAO } with a nylon monofilament suture. Cerebral cortex tissue specimens were collected after 24 hours of ischemia-reperfusion. COX-2 protein content was determined by immunohistochemistry, RT-PCR and Western blot. COX-2 mRNA expression was detected by RT-PCR. [ Results ] After 24 hours of ischemia-reperfusion, the expression of COX-2 mRNA and COX-2 in cerebral cortex was significantly increased （ P 〈 O. 05 }. Ischemic post-conditioning could significantly de- crease the cerebral COX-2 protein expression （ P 〈 0.05 ）. Compared with the sham group, the protein expression of COX-2 mRNA and COX-2 was significantly increased in the rats of I/R group and IPO group after 24 hours of ischemia-reperfusion （ P 〈 0.05 ）. But compared with I/R group, the protein expression of COX-2 mRNA and COX-2 was significantly decreased in IPO group. After ischemic postcondtioning, the levels of HSPT0 were significantly decreased （P 〈 0.05）. [ Conclusion] Ischemic pest-conditioning can decrease cerebral COX-2 expression in rats with ischemiareperfusion injury which may be part of the mechanism of brain protection.

关 键 词：缺血再灌注 缺血后处理 环氧合酶-2 

分 类 号：R461.1[医药卫生—临床医学]