脑缺血后处理对缺血再灌注脑组织细胞间黏附因子-1和髓过氧化物酶的影响

目的探讨脑缺血后处理对缺血再灌注损伤脑组织的保护机制。方法将20只SD大鼠随机分为假手术组、缺血-再灌注组、缺血后处理组及延迟缺血后处理组。采用Longa大鼠MCAO模型方法,于缺血30min、再灌注24h后应用2%氯化三苯基四氮唑染色检测梗死体积,比色法检测髓过氧化物酶活性变化,RT-PCR法检测细胞间黏附因子-1(ICAM-1)的表达。结果脑缺血后处理明显减少脑梗死体积(P0.05),降低髓过氧化物酶活性(P0.05),可抑制缺血再灌注所诱导的ICAM-1mRNA的表达(P0.05);延迟脑缺血后处理组与缺血再灌注相比无明显改变。结论脑缺血后处理有脑保护作用,其保护作用有时间依赖性,可能通过抑制细胞间黏附因子-1活性和中性粒细胞浸润起到脑保护作用。

Postconditioning attenuates cerebral ischemia-reperfusion inj ury by inhibiting intercellular adhesion molecule-1 and myeloperoxidase activity

Objective To investigate the hypothesis that ischemic postconditioning may protect cerebral ischemic tissue. Methods Twenty healthy male Sprague Dawley rats were randomly split into 4 groups:sham group,ischemia-reperfusion group, ischemic postconditioning group,delayed ischemic postconditioning group.Modles of middle cerebral artery occlusion were estab-lished with the improved Longa-Zea method.Anesthetized rats underwent 30 minutes of ischemia and 24 hours of reperfusion.The volume of cerebral infarction size was identified with 2% triphenyl tetrazolium chloride(TTC)staining.Colorimetry was used to analyze the changes of myeloperoxidase activity.Real-time PCR was used to measure the expression ICAM-1 .Results Postcondi-tioning significantly reduced infarct size(P<0.05),and myeloperoxidase activity(P<0.05).Compared with ischemia-reperfusion group,postconditioning significantly inhibited the expression of ICAM-1 .Nevertheless,delayed postconditioning didn’t have such benefit.Conclusion Postconditioning inhibits the expression of ICAM-1 and neutrophil infiltration to provide a potently anti-ische-mic protection.