白芍总苷对巨噬细胞核转录因子-κB活化的影响及其机制研究  

Effect of total glucosides of paeony on nuclear factor-κB activation in rat peritoneal macrophages

作　　者：陈刚[1] 邓小红[1] 郭莉霞[1] 刘建辉[1] 

机构地区：[1]重庆工商大学药物化学与化学生物学研究中心,重庆400067

出　　处：《中国中药杂志》2008年第6期669-671,共3页China Journal of Chinese Materia Medica

基　　金：重庆市教委科学技术研究项目(KJ060702)

摘　　要：目的:研究白芍总苷(TGP)对核转录因子-κB(NF-κB)活化的调节作用及其机制。方法:不同剂量(10,30,100,300μg.mL-1)的TGP作用于大鼠腹腔巨噬细胞2 h后,加入脂多糖(LPS)刺激20 min或1 h,Westernblot方法分别观察NF-κB抑制蛋白IκBα在胞浆中的含量及NF-κB亚基p65在胞核中的含量,同时检测NF-κB与DNA的结合活性。结果:TGP显著增加了LPS刺激后的巨噬细胞胞浆中IκBα蛋白的含量,同时显著减少了胞核中NF-κB p65蛋白含量,并对LPS诱导的NF-κB与DNA的结合活性也有明显抑制作用。结论:TGP可抑制LPS诱导的巨噬细胞NF-κB的活化,其机制与TGP抑制IκBα蛋白的降解,阻遏NF-κB p65蛋白的核转移和抑制NF-κB与DNA的结合密切相关。Objective： To study the effect of total glucosides of paeony （TGP） on lipopolysaccharides （LPS）-induced nuclear factor-κB （NF-κB） activation in macrophages. Method： Rat peritoneal macrophages were pre-treated with TGP for 2 h and stimulated with LPS for 20 min or 0. 5 h. Inhibitory κBα （IκBα） protein in the cytoplasm and NF-κB p65 protein in the nuclear were analyzed by western blot. Further, DNA binding activity of NF-κB complex was detected. Result： TGP enhanced the amounts of IκBα protein in the cytoplasm and decreased the amounts of NF-κB p65 protein in the nuclear of LPS-induced macrophages. TGP also inhibited the LPS-mediated DNA binding activity of NF-κB complex in macrophages. Conclusion： TGP can inhibit LPS-induced NF-κB activation in macrophages through arresting IκBα protein degradation, NF-κB p65 protein nuclear translocation and DNA binding activity of NF-κB complex.

关 键 词：白芍总苷 核转录因子-ΚB 抑制蛋白IκB 巨噬细胞 

分 类 号：R285[医药卫生—中药学]