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目的探讨单核细胞NF-κB的激活在COPD发病机制中的作用。方法抽取31例急性加重期组和26例稳定期组的COPD患者外周血,分离单核细胞并培养,免疫细胞化学法测定核转录因子NF-κBp65的活性表达;同时检测外周血SOD、MDA、IL-8浓度,所有患者均测定肺功能(FEV1占预计值%、FEV1/FVC)。并以15例健康志愿者作为对照组。结果LPS刺激后,急性加重期组单核细胞NF-κBp65表达显著高于稳定期组及正常组(P<0.01),稳定期组高于正常组(P<0.01)。经LPS刺激后,各组单个核细胞NF-κBp65活性均显著增高,(P<0.05);外周血单核细胞NF-κB的激活与血清IL-8、MDA水平呈正相关,而与SOD呈负相关。结论NF-κB在COPD单核细胞表达细胞因子IL-8的信号转导调控中起重要作用。
Objective To investigate the role of monocyte NF-κB activation in the pathogenesis of COPD. Methods Peripheral blood samples from 31 patients with acute exacerbation and 26 patients with stable COPD were collected and cultured. The expression of NF-κB p65 was detected by immunocytochemistry. The levels of SOD, MDA, IL-8 concentrations were measured in all patients (FEV1 predicted%, FEV1 / FVC). Fifteen healthy volunteers were used as control group. Results After LPS stimulation, the expression of NF-κBp65 in acute exacerbation group was significantly higher than that in stable group and normal group (P <0.01), and in stable group was higher than that in normal group (P <0.01). After stimulation with LPS, NF-κBp65 activity in each group of mononuclear cells was significantly increased (P <0.05). The activation of NF-κB in peripheral blood mononuclear cells was positively correlated with the levels of serum IL-8 and MDA, but not with SOD Related. Conclusion NF-κB plays an important role in the signal transduction of monocyte-derived cytokine IL-8 in COPD.