核转录因子kappaB在急性心肌梗死后心室重塑中作用研究

摘要

objection :To investigate the role of NF-κB activation in the development of the Left ventricu lar remodeling after myocardial infarction, relationship of NF-κB activation on peripheral blood mononuclear cell (PBMCs) and the level of TNF-α IL-1β. Methods: fifty-eight acute myocardial infarction patient were selected; and carried out echocardiography; and then,calculated to left ventricular end diastolic volume(refered to mathed of Simpson) 、 increase index ratio of the left ventricular end diastolic volume. According to left ventricular end diastolic volume index increasing exceed to 20 percent ,the acute myocardial infarction patient were divide in to two groups, ventricular remodeling group and no ventricular remodeling group; twenty normal human defined as control group; the activity of NF-κB was measured by immunocytochemical staining, plasma cell cytokine (TNF-αand IL-1β) were witn radio immunity assay. Results: ①Com pared witn tne normal control group and no ventricular remod eling group, NF-κB activation ,TNF-α and IL-1β levels in the ventricular remodeling after the acute myocardial in farction was bonded to be increased (P<0. 01). Discrepancy has statistical significance. ② NF-κB activation were positively correlated with the level TNF-α and IL-lβ(P<0. 05) . Conclution: Increased NF-κB activation in ventric ular remodeling after acute myocardial infarction may be upregulate cytokine . as it was, NF-κB take part in patho physiology of the heart failure and ventricles remodeling after acute myocardial infarction .%目的:探讨外周血单个核细胞(PBMCs)核因子-kappaB (NF-κB) 活化程度对急性心肌梗死(AMI)后左心室重塑(LVRM)作用及其与血浆肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)分泌的相关性.方法:选取首次AMI患者58例,进行超声心动图检查,按simpson法计算出的左心室舒张末期容积,并计算出左心室舒张末期容积指数增加率(ΔLVEDVI),以△LVEDVI>20%将患者分为心室重塑组33例和无心室重塑组25例;另取20例体检正常者为对照组.三组PBMCs 的NF-κB活性用细胞免疫化学染色检测,血浆细胞因子TNF-α,IL-1β含量由放射免疫法测定.结果:①AMI 重塑组血浆外周血PBMCs的NF-κB 核染色阳性百分率、TNF-α、IL-1β分泌表达均显著增加,高于无重塑组及健康对照组( P<0.01),差异有统计学意义.②左心室重塑组患者外周血PBMCs的NF-κB核染色阳性百分率与TNF-α、IL-1β表达均显著正相关(P<0.05).结论:AMI后心室重塑患者外周血PBMCs的NF-κB活性是明显升高的,可能是通过促进细胞因子(TNF-α、IL -1β)的分泌来参与心室重塑的发病机制.