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Endotoxin/TLR4 signaling-activate monocyte through ERK1/2 pathway
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- Author:
- No author available
- Journal Title:
- JOURNAL OF CHINESE PHYSICIAN
- Issue:
- 12
- DOI:
- 10.3760/cma.j.issn.1008-1372.2007.12.002
- Key Word:
- 受体,细胞表面;细胞外信号调节MAP激酶类;信号传导;脂多糖类;单核细胞
Abstract： 目的 探讨Toll样受体4(TLR4)与ERK1/2信号通道的相互关系.方法 收集人单核细胞体外培养,加入不同浓度的TLR4阻断剂(终浓度分别为5μg/mL,20μg/mL,30μg/mL)孵育30 min后,以终浓度10 ng/ml LPS刺激,8 h后收集上清液,ELISA法测上清液IL-6浓度.分空白组:不加LPS及TLR4阻断剂;对照组:只加终浓度10 ng/ml的LPS及RPM11640;试验组:分别加入终浓度为5μg/mL,20 μg/mL,30μg/mL的TLR4阻断剂.孵育30 min后再加入终浓度10 ng/ml的LPS刺激,20 min后Western Blot检测ERK1/2的活化.结果 LPS导致单核细胞ERK1/2的活化,TLR4受体阻断剂可阻断LPS这一效应.LPS刺激单核细胞引起上清液IL-6水平增加,TLR4受体阻断剂可显著降低IL-6水平.结论 LPS可通过单核细胞膜TLR4受体激活胞内ERK1/2信号通道.
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