摘要
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30min后，以终浓度10ng/mlLPS刺激，8h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10ng/ml的LPS及RPMI1640；试验组：分别加入终浓度为5μg/mL，20μg/mL，30μg/mL的TLR4阻断剂。孵育30min后再加入终浓度10ng/ml的LPS刺激，20min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。
Objective The aims were to explore the relation between human extracellular signal-regulated kinase （ERK1/2） and TLR4 in human monocytes. Methods Human monocytes were stimulated with various concentrations of LPS in vitro, IL-6 concentration in supernatant was measured by ELISA. Pre -incubated with various concentrations of anti-TLR4, human monocytes stimulated with LPS （10ng/mL）, then IL-6 concentration in supernatants was measured. Pre -incubated with or without anti-TLR4 antibody, then stimulated with LPS （10ng/mL） 20 minutes, ERK1/2 in human monocytes were detected by Western Blot, Results In human monocytes, LPS enhanced ERK1/2 activation, which was clearly inhibited by anti-TLR4 antibody. LPS -induced IL-6 production in human monocytes, which can be inhibited by anti-TLR4 antibody. Conclusions LPS activate ERK1/2 signal pathway through TLR4 receptor.
出处
《中国医师杂志》
CAS
2007年第12期1588-1590,共3页
Journal of Chinese Physician
关键词
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
Receptors, cell surface
Extracellular signal-regulated MAP kinase
Signal transduction
Lipopolysaccharides
Monocytes
