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目的 :探讨NFκB在维持口腔癌相关巨噬细胞炎症细胞募集表型中的作用。方法 :使用Cal27条件培养基刺激诱导小鼠原代巨噬细胞,形成口腔癌相关巨噬细胞,利用NFκB小分子抑制剂Bay11-7082抑制NFκB信号通路。利用RT-PCR、ELISA检测募集炎症细胞相关趋化因子的表达及分泌变化。采用Graph Pad Prism5对数据进行统计学分析。结果:Bay11-7082处理的巨噬细胞能够抑制Cal27条件培养基诱导原代巨噬细胞形成肿瘤相关巨噬细胞的梭状外形;同时,在m RNA水平抑制炎症细胞募集相关趋化因子MCP-1、GM-CSF、MCP-5以及CCL-5的表达上调(P<0.05)。在蛋白质水平,对NFκB的抑制能够显著减少Cal27条件培养基导致的巨噬细胞MCP-1、GM-CSF分泌增加(P<0.001)。结论 :NFκB信号通路可能参与口腔癌相关巨噬细胞募集炎症细胞表型的维持。
Objective: To investigate the role of NFκB in maintaining recruitment of inflammatory cells in oral cancer-associated macrophages. Methods: Primary murine macrophages were stimulated with Cal27 conditioned medium to form oral cancer-associated macrophages, and NFκB signaling pathway was inhibited by Bay11-7082, a small inhibitor of NFκB. The expression and secretion of chemokines in inflammatory cells were detected by RT-PCR and ELISA. Data were statistically analyzed using Graph Pad Prism5. RESULTS: The Bay11-7082-treated macrophages inhibited the spindle-shaped appearance of primary macrophages that formed tumor-associated macrophages in Cal27 conditioned medium. At the same time, they inhibited the inflammatory cells recruiting inflammatory cytokines MCP-1 , GM-CSF, MCP-5 and CCL-5 (P <0.05). At the protein level, inhibition of NFκB can significantly reduce MCP-1 and GM-CSF secretion in macrophages induced by Cal27 conditioned medium (P <0.001). Conclusion: NFκB signaling pathway may be involved in the maintenance of the phenotype of inflammatory cells recruited by oral cancer-associated macrophages.