CAJ | 학술논문

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。
목적：탐토배양화매（COX ）1、2재염증인자인기관상동맥무복류현상중적작용급궤제。방법입선44례급성심기경사（AMI）환자，측정급진PCI술전혈청염증인자（CRP、IL_6）수평，관찰기여술후무복류현상지간적관계；구건CRP자격적HCAEC모형，관찰기인、단백표체정황，탐토CRP재무복류발생발전중적작용궤제。결과무복류환자CRP、IL_6수평명현고우관주량호자，차이유통계학의의（ P＜0.05）；재CRP자격HCAEC모형중，CRP자격조COX표체수평고우대조조，응용세포외신호조절격매（ERK1／2）화안기말단격매（JNK1／2）억제제후COX표체현저강저，차이균유통계학의의（ P＜0.01）。결론 CRP가통과격활COX염증통로，유발AMI급진PCI술후무복류현상적산생。
Objective To explore the effects and molecular mechanisms of cyclooxygenase (COX1 ,2) on inflammatory factor induc-ing 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 sig-nificant 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 path-ways of COX inflammation ,CRP could cause no_reflow after AMI emergency PCI.