摘要
目的 :研究心肌缺血再灌注时中性粒细胞 (PMN)内核因子 -kB活性变化与中性粒细胞细胞间粘附分子 (ICAM -1)表达及中性粒细胞心肌浸润的关系。方法 :新西兰兔 2 4只分为 :(1)缺血再灌注组 (IR) ,(2 )IR +RDTC组 ,(3)假手术对照组 ,并分缺血前 ,再灌注后 30、 6 0、 90、 12 0、 2 4 0、 36 0min时相点。用流式细胞仪检测PMNsICAM - 1的表达 ,凝胶电泳迁移率分析检测NF -kB的活性 ,酶法测定PMNs浸润数。结果 ,心肌再灌注 30nin后NF kB活性开始增高 ,12 0min达到高峰 ,之后活性下降 ;PMNsICAM - 1的表达在心肌再灌注 12 0min开始增高 ,并与PMNs浸润数升高有相关性 ;PDTC能抑制NF -kB的活化及PMNsICAM - 1的表达和PMNs浸润。结论 :心肌缺血再灌注时刺激NF -kB的活化 ,启动PMNsICAM - 1的表达而参与缺血再灌注损伤的发生过程。
Objective:To study the relationships among the activation of nuclear factor-kappaB (NF-kB), expression of intercellular adhesion moleculer (ICAM-1) and infiltration of polymorphonuclear neutriphils(PMNs) in myocardial ischemic-reperfusion(IR). Method :Twenty four Newzeland rabbits were divided into three groups:IR, IR+PDTC (control) and pyrrolidine dithiocarbamate (PDTC)group. The blood and ischemic myocardial samples were studied before ischemia and 30, 60, 90, 120, 240, 360 min after ischemic reperfusion. The expression levels of ICAM-1 were evaluated by flucyto, activation of NF-kB by EMSA, the number of infiltrated PMNs was measured with MPO enzyme marker method. Result : After IR 30 min, activation of NF-kB increased significantly, reached a peak at 120 min and then decreased; the expression levels of ICAM-1 increased at 120 min and had postive correlation to the number of infiltrated PMNs. In IR+PDTC group, PDTC could inhibt the activation of NF-kB,expresion of ICAM-1 and infiltration of PMNs. Conclusion : The inducible activation of NF-kB starts ICAM-1 expression of PMNs and it is an important factor in myocardial ischemic-reperfusion injury.
出处
《西南国防医药》
CAS
2002年第1期17-20,共4页
Medical Journal of National Defending Forces in Southwest China
