范虞琪, 魏立, 王君. NF-κB在铁负荷过低上调炎症因子中的作用[J]. 心脏杂志, 2011, 23(2): 205-208.
    引用本文: 范虞琪, 魏立, 王君. NF-κB在铁负荷过低上调炎症因子中的作用[J]. 心脏杂志, 2011, 23(2): 205-208.
    Effect of nuclear factor (NF)-κB on induction of EMMPRIN by excessive low iron load in macrophages and foam cells[J]. Chinese Heart Journal, 2011, 23(2): 205-208.
    Citation: Effect of nuclear factor (NF)-κB on induction of EMMPRIN by excessive low iron load in macrophages and foam cells[J]. Chinese Heart Journal, 2011, 23(2): 205-208.

    NF-κB在铁负荷过低上调炎症因子中的作用

    Effect of nuclear factor (NF)-κB on induction of EMMPRIN by excessive low iron load in macrophages and foam cells

    • 摘要: 目的: 探讨核转录因子(NF)-κB在铁负荷过低上调巨噬细胞、泡沫细胞炎症因子反应中的作用。方法: 将巨噬细胞和泡沫细胞给予NF-κB抑制剂预处理,加入或不加入铁离子鳌合剂去铁胺(DFO)继续培养24 h,用Western blot测定细胞中细胞外基质金属蛋白酶诱导因子(EMMPRIN)蛋白的表达。于巨噬细胞和泡沫细胞中加入DFO刺激,用Western blot测定细胞核中NF-κB p65蛋白的表达。将巨噬细胞和泡沫细胞给予p38 MAPK信号通路抑制剂或视黄醛x受体(RXR)的天然配体预处理,加入DFO刺激,用Western blot测定细胞核中NF-κB p65蛋白的表达。结果: NF-κB抑制剂可抑制DFO对巨噬细胞、泡沫细胞中EMMPRIN上调的作用。DFO可促进巨噬细胞、泡沫细胞细胞核中NF-κB p65蛋白的表达。p38 MAPK通路抑制剂或RXR配体可抑制DFO对NF-κB p65蛋白水平上调的作用。结论: NF-κB 参与了铁负荷过低上调巨噬细胞和泡沫细胞中EMMPRIN表达的过程。RXR配体对铁负荷过低上调炎症反应的抑制作用,同其抑制NF-κB激活有关。

       

      Abstract: AIM: To investigate the effect of NF-κB on the induction of EMMPRIN by excessive low iron load in macrophages and foam cells. METHODS: Thp-1 derived macrophages and foam cells were pre-treated with NF-κB inhibitor and then were stimulated with/without desferrioxamine (DFO) for 24 h. EMMPRIN expression was assayed by Western blot. Cells were stimulated with DFO for different time periods and nuclear NF-κB p65 protein levels were then assayed by Western blot. Cells were pre-treated with p38 MAPK inhibitors or RXR ligand and nuclear NF-κB p65 protein levels were assayed again by Western blot. RESULTS: NF-κB inhibitor blocked the induction of EMMPRIN by DFO stimulation, DFO enhanced nuclear NF-κB p65 protein levels in macrophages and foam cells and p38 MAPK inhibitor and RXR ligand significantly blocked DFO upregulation of NF-κB p65. CONCLUSION: NF-κB is involved not only in the excessive low iron load upregulation of EMMPRIN expression, but also in the RXR ligand downregulation of inflammatory factor in macrophages and foam cells.

       

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