核因子κB对维持口腔癌相关巨噬细胞炎症细胞募集表型的作用

doi:10.19439/j.sjos.2017.02.005

上海口腔医学 ›› 2017, Vol. 26 ›› Issue (2): 151-155.doi: 10.19439/j.sjos.2017.02.005

核因子κB对维持口腔癌相关巨噬细胞炎症细胞募集表型的作用

周笑天¹, 陈东¹, 金震宁¹, 黄珂¹, 林洁^1,2, 门乙^1,3*, 李春洁^1,3*

1.口腔疾病研究国家重点实验室,四川成都 610041;
2.四川大学华西口腔医学院口腔麻醉科,3.头颈肿瘤外科,四川成都 610041

收稿日期:2016-03-05 修回日期:2016-09-13 出版日期:2017-04-25 发布日期:2017-05-04
通讯作者: 门乙,E-mail: yurimen@163.com;李春洁,E-mail: lichunjie@scu.edu.cn。^*共同通信作者
作者简介:周笑天（1994-）,男,学士,E-mail：340075992@qq.com
基金资助:
2014年四川大学青年教师科研启动基金（2014SCU11999）; 2015年四川大学“大学生创新创业训练计划”资助（201510611949）

Investigation of the effect of nuclear factor κB on inflammatory cell recruitment phenotype of oral cancer associated macrophage

ZHOU Xiao-tian¹, CHEN Dong¹, JIN Zhen-ning¹, HUANG Ke¹, LIN Jie^1,2, MEN Yi^1,3, LI Chun-jie^1,3

1.State Key Laboratory of Oral Disease. Chengdu 610041;
2.Department of Dental Anesthesia, 3.Department of Head and Neck Oncology, West China Hospital of Stomatology, Sichuan University. Chengdu 610041, Sichuan Province, China

Received:2016-03-05 Revised:2016-09-13 Online:2017-04-25 Published:2017-05-04

摘要/Abstract

摘要： 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GraphPadPrism5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mRNA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。

关键词: 炎症细胞募集, 口腔癌, 核因子κB, 巨噬细胞

Abstract: PURPOSES: To explore the ability of nuclear factor κB (NFκB) in sustaining inflammatory cell recruitment phenotype of oral cancer associated macrophages, by using NFκB inhibitor(-Bay11-7082). METHODS: By primary culture, murine macrophages were harvested. Cal27 conditioned medium (CM) and Bay11-7082 were applied for stimulation of the macrophages. RT-PCR and ELISA were used for detecting the inflammatory cell recruitment related chemotactic factors. GraphPadPrism5 was used for statistical analysis. RESULTS: Bay11-7082 prevented the contour change into a spindle shape via Cal 27 CM. It also attenuated MCP-1, GM-CSF, MCP-5 and CCL-5 mRNA increase after Cal 27 CM stimulation (P<0.05). At protein level, impeding NFκB activation could significantly prevent MCP-1 and GM-CSF secretion from oral cancer associated macrophage (P<0.001). CONCLUSIONS: NFκB signaling may play a key role in sustaining the inflammatory cell recruitment phenotype of oral cancer associated macrophages.

Key words: Inflammatory cell recruitment, Mouth neoplasm, Nuclear factor κB, Macrophage

中图分类号:

R739.8

周笑天, 陈东, 金震宁, 黄珂, 林洁, 门乙, 李春洁. 核因子κB对维持口腔癌相关巨噬细胞炎症细胞募集表型的作用[J]. 上海口腔医学, 2017, 26(2): 151-155.

ZHOU Xiao-tian, CHEN Dong, JIN Zhen-ning, HUANG Ke, LIN Jie, MEN Yi, LI Chun-jie. Investigation of the effect of nuclear factor κB on inflammatory cell recruitment phenotype of oral cancer associated macrophage[J]. Shanghai Journal of Stomatology, 2017, 26(2): 151-155.

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核因子κB对维持口腔癌相关巨噬细胞炎症细胞募集表型的作用

Investigation of the effect of nuclear factor κB on inflammatory cell recruitment phenotype of oral cancer associated macrophage

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