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为观察白细胞介素－１０（ＩＬ－１０）和地塞米松（Ｄｅｘ）对核因子－κＢ（ＮＦ－κＢ）的活化及α肿瘤坏死因子（ＴＮＦα）释放的影响，采用分离培养的人外周血单个核细胞（ＰＢＭＣ），分为正常对照组、脂多糖（ＬＰＳ）刺激组、ＩＬ－１０ 和Ｄｅｘ 干预组。用凝胶电泳迁移率改变分析法（ＥＭＳＡ）检测ＰＢＭＣ核提取物中ＮＦ－κＢ的活性，ＥＬＩＳＡ法检测培养上清中ＴＮＦα的含量。结果发现，ＬＰＳ刺激后１ｈ ＮＦ－κＢ活性显著高于正常对照组（Ｐ＜ ０．０１），ＴＮＦα的释放显著增加（Ｐ＜ ０．０１）；ＩＬ－１０、Ｄｅｘ 显著抑制ＮＦ－κＢ活性（Ｐ＜ ０．０１） ，也显著抑制ＴＮＦα的释放。提示抑制ＮＦ－κＢ激活和ＴＮＦα的产生可能是ＩＬ－１０ 和Ｄｅｘ 发挥抗炎作用的重要机制之一
To observe the effects of interleukin-10 (IL-10) and dexamethasone (Dex) on the activation of NF-κB and the release of TNFα, human peripheral blood Mononuclear cells (PBMC) were divided into normal control group, lipopolysaccharide (LPS) stimulation group, IL-10 and Dex intervention group. The activity of NF-κB in PBMC nuclear extracts was detected by gel electrophoretic mobility shift assay (EMSA). The content of TNFα in culture supernatants was detected by ELISA. The results showed that the activity of NF-κB 1 h after LPS stimulation was significantly higher than that of the normal control group (P <0.01), and the release of TNFα was significantly increased (P <0.01); IL-10 and Dex significantly inhibited the activity of NF- P <0.01), but also significantly inhibited the release of TNFα. It is suggested that the inhibition of NF-κB activation and TNFα production may be one of the important mechanisms by which IL-10 and Dex play an anti-inflammatory role