中性粒细胞在心肌缺血再灌注中ICAM-1表达及核转录调控的实验研究

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24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、60、90、120、240、360min时相点。用流式细胞仪检测PMNs ICAM-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，120min达到高峰，之后活性下降；PMNs ICAM-1的表达在心肌再灌注120min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PMNs ICAM-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PMNs ICAM-1的表达而参与缺血再灌注损伤的发生过程。

EXPERIMENTAL SUTDY ON EXPRESSION AND NUCLEAR TRANSCRPTIONAL REGULATION OF ICAM-1 OF PMMS IN MYOCARDIAL ISCHEMIC-REPERFUSION INJURY

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.