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中国临床药理学与治疗学 ›› 2009, Vol. 14 ›› Issue (9): 1023-1027.

• 基础研究 • 上一篇    下一篇

地塞米松对树突状细胞Toll 样受体4信号通路的影响

伍香玲1, 何小魁1, 李波1, 胡永秀2   

  1. 1首都医科大学基础医学院免疫学系,2基础医学实验教学中心, 北京100069
  • 收稿日期:2009-05-19 修回日期:2009-09-08 发布日期:2020-11-03
  • 通讯作者: 李波, 男, 博士, 副教授, 研究方向:免疫细胞信号转导。Tel:010-83911438 E-mail: mailboli@yahoo.com.cn;胡永秀,女, 硕士, 教授, 硕士研究生导师, 研究方向:移值免疫。Tel:010-83911742 E-mail: yxh601@yahoo.com.cn
  • 作者简介:伍香玲, 女, 硕士研究生, 研究方向:移植免疫。Tel:13811243166 E-mail:xiangling2001@163.com
  • 基金资助:
    北京市教委科技发展计划项目(KM200710025005)

Effects of dexamethasone on toll-like receptor 4 mediated signaling pathways in mice dendritic cells

WU Xiang-ling, HE Xiao-kui, LI Bo, HU Yong-xiu   

  1. Department of Immunology, School of Basic Medical Science, Capital Medical University, Beijing 100069, China
  • Received:2009-05-19 Revised:2009-09-08 Published:2020-11-03

摘要: 目的: 观察地塞米松对树突状细胞(dendriticcells, DC) 表面分子Toll 样受体4(toll-like receptor4, TLR4) 及转录因子NF-κB 表达的影响, 以探讨地塞米松抑制DC 分化成熟和抗原提呈功能的作用机制。方法: 常规培养小鼠DC, 在培养体系中加入地塞米松作用后, 通过流式细胞术分析DC TLR4 表达情况;凝胶电泳迁移实验(EMSA) 分析DC NF-κB 活化情况。结果: 地塞米松以剂量依赖方式抑制NF-κB 表达, 但对TLR4 表达无抑制作用。结论: 地塞米松影响DC 分化成熟和抗原提呈功能的机制可能与其对NF-κB 活化的抑制作用有关。

关键词: 树突状细胞, 地塞米松, Toll 样受体4, NF-κB

Abstract: AIM: To observe the effects of dexamethasone on the expression of toll-like receptor 4 (TLR4) and the activation of NF-κB of dendritic cells (DC), and investigate the mechanism of dexamethasone suppressing differentiation, maturation, and function of DC. METHODS: DC generated from C57BL/6 murine bone marrow cells were induced by GM-CSF and IL-4.Dexamethasone was added in the DC's culture system, the cells were analyzed by flow cytometry (FCM) to determine the expression of TLR4 &CD11c, and by electrophoretic mobility shift assay (EMSA) to verify the activation of transcription factor NF-κB of DC. RESULTS: Dexamethasone could suppress the expression of CD11c and the activation of NF-κB with a dose-effect relationship in DC, but it could not suppress the expression of TLR4 of DC. CONCLUSION: The mechanism of dexamethasone involved in inhibition of differentiation, maturation, and function of DC is perhaps related to suppression of NF-κB activation.

Key words: dendritic cells, dexamethasone, tolllike receptor 4, nuclear factor kappa B

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