炎症反应在多壁碳纳米管致胸膜间皮细胞恶性转化中的作用

Role of inflammation in malignant transformation of pleural mesothelial cells induced by multiwalled carbon nanotubes

  • 摘要:
    目的 探讨巨噬细胞产生的炎症反应在多壁碳纳米管(multi-walled carbon nanotubes,MWCNTs)致胸膜间皮细胞恶性转化中的作用及可能的分子机制。

    方法 分别在有(+)或无(-)MWCNTs染毒情况下,利用人胸膜间皮细胞(Met5A)和巨噬细胞共培养以及Met5A单独培养两种模式培养细胞3个月后,检测各组胸膜间皮细胞的增殖、迁移、克隆形成能力,及胸膜间皮细胞核因子-κBNF-κB)、白细胞介素-6(IL-6)、信号转导和转录激活因子3(STAT3)基因表达水平的变化。

    结果 与单独培养(+)组和单独培养(-)组比较,共培养(+)组间皮细胞的光密度值、穿膜的细胞数目、形成的细胞克隆数目均明显增加,差异具有统计学意义(P < 0.05)。单独培养(+)组与单独培养(-)组比较,间皮细胞的光密度值、穿膜的细胞数目、形成的细胞克隆数目增加,差异具有统计学意义(P < 0.05)。与单独培养(+)组及单独培养(-)组比较,共培养(+)组间皮细胞的NF-κBIL-6STAT3基因表达水平明显升高,差异具有统计学意义(P < 0.05)。

    结论 MWCNTs可促进胸膜间皮细胞的恶性转化,且巨噬细胞产生的炎症反应可增强MWCNTs致胸膜间皮细胞的恶性转化能力。

     

    Abstract:
    Objective To investigate the role of inflammation caused by macrophages and the possible mechanisms in the malignant transformation of pleural mesothelial cells induced by multi-walled carbon nanotubes (MWCNTs).

    Methods The proliferation, migration and colony formation ability of pleural mesothelial cells and the gene expression levels of nuclear factor kappa B (NF-κB), interleukin 6 (IL-6), and signal transducer and activator of transcription 3 (STAT3) in pleural mesothelial cells were detected after three months of co-culture of mesothelial cells Met5A and macrophages and the separate culture of Met5A cells in the presence (+) or absence (-) of MWCNTs.

    Results The proliferation, migration, and clony formation ability of mesothelial cells in the co-culture (+) group were significantly enhanced compared with those in the separate culture (+) group and the separate culture (-) group (P < 0.05). The three in dicators in the co-culture (+) group were also enhanced compared with those of the separate culture (-) group (P < 0.05). The gene expression levels of NF-κB, IL-6, and STAT3 in the co-culture (+) group were significantly increased compared with those in the separate culture (+) group and the separate culture (-) group (P < 0.05).

    Conclusion MWCNTs can promote malignant transformation of pleural mesothelial cells, furthermore this effect can be enhanced by the inflammation caused by macrophages.

     

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