目的观察溃结灵对白介素-1β(IL-1β)刺激的Caco-2炎症细胞模型核因子抑制蛋白-κB(IκBα)基因表达及蛋白表达的作用，对其抗溃疡性结肠炎(UC)作用机制进行探讨。方法将生长融合至70 %～80 %的Caco-2细胞分为7个组:正常对照组、模型组、蛋白酶抑制剂组、阳性药柳氮磺胺吡啶组(SASP)及溃结灵高、中、低剂量组。IL-1β刺激细胞建立炎症模型，收集细胞标本。采用实时荧光定量PCR方法检测Caco-2细胞IκBα的基因表达，Western blot方法检测其蛋白表达。结果IL-1β刺激的Caco-2炎症细胞中，模型组IκBα基因表达明显低于正常对照组(P < 0.05)，溃结灵中剂量组IκBα基因表达明显高于模型组(P < 0.05)；IL-1β刺激的Caco-2细胞炎症中，模型组IκBα蛋白表达低于正常对照组，但差异无统计学意义(P ＞ 0.05)，而溃结灵高剂量组IκBα蛋白表达明显高于模型组(P < 0.01)。结论溃结灵对IL-1β刺激的Caco-2炎症细胞IκBα基因和蛋白的表达有上调作用，其抗UC作用的机理可能为抑制IκBα蛋白的降解，最终抑制NF-κB的活化，减轻炎症反应。

Objective To observe the effect of Kuijieling Decoction(KD)on nuclear factor profilin kappa B(IκBα)gene and protein expression in Caco-2 cell model induced by interleukin-1β(IL-1β)，and to explore its possible mechanism. Methods Caco-2 cells in the growth density of 70%-80% were divided into seven groups:normal group，model group，proteasome inhibitor bortezomib group，positive drug salazosulfapyridine(SASP)group，and high-，middle- and low-dose HD groups. The cells were stimulated by IL-1β for the establishment of cell model of inflammation. Real-time quantitative PCR and Western blotting technique were used to detect gene and protein expression of IκBα，respectively. Results The relative gene expression level of IκBα in the model group was lower than that in the normal group(P < 0.05)，and was significantly higher in the middle-dose KD group than that in the model group(P < 0.05). The relative protein expression level of IκBα was lower in the model group than that in the normal group，but the difference was insignificant(P > 0.05). High-dose KD group had significantly higher IκBα protein expression level than the model group(P < 0.01). Conclusion KD has an effect on the up-regulation of the gene and protein expression levels of IκBα in Caco-2 cell induced by IL-1β，and its anti-ulcerative colitis mechanism is probably related to reducing the degradation of IκBα，and finally inhibiting the activation of NF-κB and relieving inflammatory reaction.

R285.5

国家自然科学基金资助项目(30873421)。