中文摘要：

目的：研究肾上腺素对脂多糖（LPS）诱导的小鼠单核巨噬细胞株RAW264．7中促炎介质[肿瘤坏死因子（TNF—α）、一氧化氮（NO）、环加氧酶-2（COX-2）]和抗炎介质[血红素氧化酶-1（HO—1）、白介素10（IL-10）]表达及NF—κB活化的影响。方法：以10μg／U的LPS刺激体外培养的RAW264．7细胞作为炎症模型，加入不同浓度的肾上腺素（1、5、10、50μmol／L）孵育24h后，收集培养上清并提取细胞总蛋白，酶联免疫法测定上清中TNF—α、IL—10浓度，Griess法检测上清NO含量（以NO2^-／NO3^-表示），免疫印迹法检测细胞总蛋白中COX-2、HO—1、IκB—α的含量。结果：10μg／U的LPS明显诱导TNF—α、NO（NO2^-／NO3^-）、COX-2、IL-10及HO—1的产生；LPS＋肾上腺素组与LPS单独作用组相比促炎介质TNF—α、NO（NO2^-／NO3^-）、COX-2的表达量显著下降，而抗炎介质IL-10、HO—1的表达却明显增强；肾上腺素与LPS共同作用组中IκB—α的含量与单独LPS作用组相比无明显差异。结论：肾上腺素下调LPS诱导的巨噬细胞中促炎介质的表达同时促进抗炎介质的表达，这种效应并不通过影响NF—κB的活化来实现。

英文摘要：

AIM： To investigate the effect of epinephrine on LPS - induced pro - inflammatory mediators （TNF - α, NO and COX-2） and anti - inflammatory mediators （HO- 1 and IL- 10） production in murine macrophage RAW264.7 cells, and to determine whether these effect is due to the influence of epinephrine on NF - κB activation.METHODS： RAW264.7 cells were cultured in vitro with 10 μg/L LPS in the absence or presence of epinephrine at variant concentrations （1, 5, 10, 50μmol/ L） for 24 hours, then the supematants was collected for measuring TNF-α and IL- 10 by ELISA and Griess reagent was used to measure NO （NO2^-/NO3^- ） concentration. At the same time point, cells were harvested and COX - 2, HO - 1 and IκB - α was detected by Western blotting. RESULTS： 10μg/L LPS significantly induced the production of TNF - α, NO （NO2^-/NO3^- ）, COX - 2, HO - 1 and IL- 10. When epinephrine was added into the medium together with LPS, the pro - inflammatory mediators production was decreased in a dose- dependent manner, however, anti - inflammatory mediators HO- 1 and IL- 10 expression was enhanced by epinephrine. Epinephrine has no significant effect on IκB - α degradation in LPS - activated RAW264.7 cells. CONCLUSION： Epinephrine down- regulates LPS- induced pro- inflammatory mediator expression while promotes anti- inflammatory mediator production in routine macrophages. These effect seems to be independent of NF-κB activation.