Chen Gang, Deng Xiao-Hong, Guo Li-Xia, Liu Jian-Hui
Research Center of Medical Chemistry and Chemical Biology, Chongqing Technology and Business University, Chongqing 400067, China.
Zhongguo Zhong Yao Za Zhi. 2008 Mar;33(6):669-71.
To study the effect of total glucosides of paeony (TGP) on lipopolysaccharides (LPS)-induced nuclear factor-kappaB (NF-kappaB) activation in macrophages.
Rat peritoneal macrophages were pre-treated with TGP for 2 h and stimulated with LPS for 20 min or 0.5 h. Inhibitory kappaBalpha (IkappaBalpha) protein in the cytoplasm and NF-kappaB p65 protein in the nuclear were analyzed by western blot. Further, DNA binding activity of NF-kappaB complex was detected.
TGP enhanced the amounts of IkappaBalpha protein in the cytoplasm and decreased the amounts of NF-kappaB p65 protein in the nuclear of LPS-induced macrophages. TGP also inhibited the LPS-mediated DNA binding activity of NF-kappaB complex in macrophages.
TGP can inhibit LPS-induced NF-kappaB activation in macrophages through arresting IKBalpha protein degradation, NF-kappaB p65 protein nuclear translocation and DNA binding activity of NF-kappaB complex.
研究芍药总苷（TGP）对脂多糖（LPS）诱导的巨噬细胞核因子-κB（NF-κB）激活的影响。
用TGP预处理大鼠腹腔巨噬细胞2小时，然后用LPS刺激20分钟或0.5小时。通过蛋白质免疫印迹法分析细胞质中的抑制性κBα（IkBα）蛋白和细胞核中的NF-κB p65蛋白。此外，检测NF-κB复合物的DNA结合活性。
TGP增加了LPS诱导的巨噬细胞细胞质中IkBα蛋白的量，减少了细胞核中NF-κB p65蛋白的量。TGP还抑制了LPS介导的巨噬细胞中NF-κB复合物的DNA结合活性。
TGP可通过阻止IκBα蛋白降解、NF-κB p65蛋白核转位和NF-κB复合物的DNA结合活性来抑制LPS诱导的巨噬细胞NF-κB激活。
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