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为观察脂多糖（ＬＰＳ）处理单核细胞（Ｍ）后对核因子－κＢ抑制蛋白（ＩκＢα）降解，ＮＦ－κＢ活化及α肿瘤坏死因子（ＴＮＦα）表达的影响，分离、培养Ｍ，分为正常对照组和ＬＰＳ刺激组（ＬＰＳ１０μｇ／ｍ ｌ）；分别在刺激前（０）、刺激后１５、３０ｍ ｉｎ 和１、２、４ｈ，留取Ｍ 和细胞培养上清。检测Ｍ ＩκＢ水平和核提取物中ＮＦ－κＢ的活性和细胞培养上清中ＴＮＦα的含量。结果发现，ＬＰＳ刺激组ＩκＢ水平１５ｍ ｉｎ 开始降低，３０ｍ ｉｎ 降到最低值；ＮＦ－κＢ活性在３０ｍ ｉｎ～４ｈ 显著增高，峰值在刺激后１～２ｈ；ＬＰＳ刺激后１～２ｈ，ＴＮＦα显著升高（Ｐ＜ ０．０１），峰值在刺激后１ｈ。ＮＦ－κＢ活性与ＴＮＦα含量在刺激后１ｈ 峰值呈显著正相关（ｒ＝ ０．９０１，Ｐ＜ ０．０１）。结果提示， ＬＰＳ可诱导Ｍ 的ＩκＢ降解和ＮＦ－κＢ激活。ＮＦ－κＢ活化后可导致ＴＮＦα的基因转录和表达增加。
To observe the effect of lipopolysaccharide (LPS) treatment of monocytes (M) on the degradation of nuclear factor-kappa B inhibitor (IκBα), the activation of NF-κB and the expression of α tumor necrosis factor (TNFα) Normal control group and LPS stimulation group (LPS 10μg / ml); M and cell culture supernatants were collected before stimulation (0), 15,30 and 1, 2 and 4 hours after stimulation. The level of M IκB and the activity of NF-κB in nuclear extracts and the level of TNFα in cell culture supernatants were determined. Found, LPS stimulation IκB levels 15m in begins to decrease, 30m in a minimum value; NF-κB activity was increased markedly in 30m in ~ 4h, a peak at 1 ~ 2h after stimulation; after LPS stimulation 1 ~ 2h, TNFα significantly liter High (P <0.01), peaked 1h after stimulation. There was a significant positive correlation between NF-κB activity and TNFα level at 1 hour after stimulation (r = 0.901, P <0.01). The results suggest that LPS can induce M IκB degradation and NF-κB activation. Activation of NF-κB results in increased gene transcription and expression of TNFα.