环氧化酶在炎症因子引起冠状动脉无复流现象中的作用机制研究

Mechanism of Action of Cyclooxygenase in Inflammatory Factor Inducing No_ reflow of Coronary Artery

目的探讨环氧化酶(COX)1、2在炎症因子引起冠状动脉无复流现象中的作用及机制。方法入选44例急性心肌梗死(AMI)患者,测定急诊PCI术前血清炎症因子(CRP、IL_6)水平,观察其与术后无复流现象之间的关系;构建CRP刺激的HCAEC模型,观察基因、蛋白表达情况,探讨CRP在无复流发生发展中的作用机制。结果无复流患者CRP、IL_6水平明显高于灌注良好者,差异有统计学意义(P<0.05);在CRP刺激HCAEC模型中,CRP刺激组COX表达水平高于对照组,应用细胞外信号调节激酶(ERK1/2)和氨基末端激酶(JNK1/2)抑制剂后COX表达显著降低,差异均有统计学意义(P<0.01)。结论 CRP可通过激活COX炎症通路,诱发AMI急诊PCI术后无复流现象的产生。

Objective To explore the effects and molecular mechanisms of cyclooxygenase（ COX1,2） on inflammatory factor inducing no-reflow of coronary artery. Methods Forty- four patients were enrolled. The serum inflammatory factors levels（ CRP and IL-6） of preoperative PCI were measured with the drug-eluting stents,to investigate whether the inflammatory factor differs in no-reflow and normal reflow patients. Human coronary artery endothelial cells（ HCAEC） model,which were simulated by CPR,were cultivated to analyze the expression of gene and protein,and to discuss the mechanism of action of CRP in no-reflow situation. Results The CRP and IL-6 levels of patients in no-reflow group were significantly higher than those in normal reflow group,there were statistically significant differences（ P〈0. 05）. In the CRP simulated HCAEC model,the expressions of COX in CRP-simulated group was higher than that of the control group,and it decreased significantly after using the extracellular signal-regulated kinase（ ERK1 /2） and jun n-terminal kinase（ JNK 1 /2） inhibitor,there were statistically significant differences（ P〈0. 01）. Conclusions By activating the pathways of COX inflammation,CRP could cause no-reflow after AMI emergency PCI.