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目的:研究心肌缺血—再灌注时中性粒细胞(PMN)核因子—kB(NF—kB)活性、细胞间粘附分子(ICAM—1)表达、中性粒细胞粘附浸润的变化及三七总皂甙的心肌保护作用。方法:新西兰兔124只分为:(1)缺血—再灌注组;(2)三七总皂甙预处理组(PNS预处理组);(3)假手术对照组;每组又分缺血前(0)、再灌注后30、60、90、120、240、360分钟时相点。用流式细胞仪检测中性粒细胞ICAM—1的表达,凝胶电泳迁移率分析检测NF—kB的活性,测定中性粒细胞与脐静脉内皮细胞(EC—340)的粘附率,用髓过氧化酶法(MPO)定量测定心肌组织中浸润的中性粒细胞。结果:在缺血—再灌注组中心肌再灌注30分钟后NF—kB活性开始增高,120分钟达到高峰,之后活性下降;中性粒细胞ICAM—1的表达在心肌再灌注120分钟开始增高,并与中性粒细胞的粘附率升高及心肌浸润增加有相关性;在PNS预处理组,PNS能抑制NF—kB的活化、中性粒细胞ICAM—1的表达和中性粒细胞的粘附及心肌浸润。结论:心肌缺血—再灌注时刺激NF—kB的活化,启动中性粒细胞ICAM—1的表达而参与缺血—再灌注损伤的发生过程:三七总皂甙能抑制中性粒细胞NF—kB的活化,减少细胞间粘附分子表达及中性粒细胞粘附浸润而起到心肌保护的作用。
OBJECTIVE: To study the changes of neutrophils (PMN) nuclear factor-kappa B (NF-kB) activity, intercellular adhesion molecule (ICAM-1) expression, and neutrophil adhesion infiltration during myocardial ischemia-reperfusion. The Protective Effect of Panax Notoginseng Saponins on Myocardium. Methods: 124 New Zealand rabbits were divided into: (1) ischemia-reperfusion group; (2) panax notoginseng preconditioning group (PNS pretreatment group); (3) sham operation control group; each group was divided into ischemia Before (0), 30, 60, 90, 120, 240, 360 minutes after reperfusion. The expression of ICAM-1 in neutrophils was detected by flow cytometry, the activity of NF-kB was measured by electrophoretic mobility shift assay, and the adhesion rate of neutrophils to umbilical vein endothelial cells (EC-340) was measured. Myeloperoxidase (MPO) was used to quantify infiltrating neutrophils in myocardial tissue. Results: Ischemia - reperfusion myocardial reperfusion 30 minutes began to increase the activity of NF-kB 120 minutes to reach the peak, then the activity decreased; ICAM-1 expression in neutrophils in myocardial reperfusion 120 minutes began to increase, It is also related to the increase of adhesion rate of neutrophils and increase of myocardial infiltration. In PNS pretreatment group, PNS can inhibit the activation of NF-kB, the expression of neutrophil ICAM-1, and the expression of neutrophils. Adhesion and myocardial infiltration. Conclusion: myocardial ischemia - stimulation of NF-kB activation of reperfusion, ICAM-1 expression promoter neutrophils participate ischemia - reperfusion injury occurs during: panax notoginseng saponins can inhibit neutrophil NF- The activation of kB reduces the expression of intercellular adhesion molecules and neutrophil adhesion infiltration and plays a role in myocardial protection.