中文摘要：

目的：研究金雀异黄素对脂多糖（LPS）诱导巨噬细胞RAW264.7分泌功能的影响,探讨金雀异黄素抗炎作用及其机制,为临床应用提供理论基础。方法：用脂多糖诱导巨噬细胞株Raw264.7建立体外细胞炎症模型,金雀异黄素与巨噬细胞株Raw264.7温孵1h后,加入100ng·mL-1脂多糖以诱导巨噬细胞的活化,采用Griess试剂检测细胞培养液中NO的含量,通过双抗体夹心酶联分析法和细胞转染技术观察不同浓度金雀异黄素对脂多糖刺激巨噬细胞分泌细胞因子TNF-α、IL-6和IL-10含量及对核转录因子NF-κB和AP-1表达的影响。结果：金雀异黄素（4～111μmolL-1）能明显抑制脂多糖刺激巨噬细胞生成一氧化氮产生（P〈0.05）;显著抑制脂多糖诱导巨噬细胞分泌细胞因子TNF-α、IL-6和IL-10（P〈0.01）,并能抑制核转录因子NF-κB和AP-1的表达。结论：本实验证明了金雀异黄素有抗炎作用,其能显著降低脂多糖诱导巨噬细胞分泌NO及细胞因子TNF-α、IL-6和IL-10的释放,通过抑制这些炎症因子的释放来达到抗炎作用,金雀异黄素抑制核转录因子NF-κB和AP-1的表达来实现的。

英文摘要：

Objective： To investigate effects of genistein on the NO and cytokine production of murine macrophage Raw 264. 7 stimulated by LPS Methods： Genistein pretreat macrophage 1 hour before LPS stimulation for different time points. The NO2-production was tested by Griess reagents and cytokines were dectected by ELISA,The expression of transcrpiton factor of NF-κB and AP-1 was investigated by Reporter cell line Raw BlueTM cells. Results： genistein （4-111μmolL-1）significantly inhibit NO production（P 0. 05） as well as cytokines production （TNF-α、IL-6 and IL-10） （P 0. 01） by LPS. Genistein can dramaticly inhibit the expression of transcription factor NF-κB and AP1. Conclusion： Genistein shows a promininet anti-inflammatory property due to its effect . on the NO and cytokines production by LPS stimulated macrophage. The effect is due to inhibition the expression of transcription factor NF-κB and AP-1.