基础医学与临床 ›› 2010, Vol. 30 ›› Issue (11): 1206-1209.

• 研究论文 • 上一篇    下一篇

脂多糖通过NF-κB途径调节大鼠星形胶质细胞Toll样受体表达

张红 李学忠 白龙梅 杨亚萍 周媛 刘春风   

  1. 镇江市第一人民医院 镇江市第一人民医院 苏州大学衰老和神经疾病实验室 苏州大学衰老和神经疾病实验室 苏州大学衰老和神经疾病实验室
  • 收稿日期:2009-11-03 修回日期:2010-03-23 出版日期:2010-11-05 发布日期:2010-11-05
  • 通讯作者: 李学忠

Lipopolysaccharides regulated the expression of toll-like receptors in astrocytes through NF-κB signal pathway

Hong ZHANG, Xue-zhong LI, Long-mei BAI, Ya-ping YANG, Yuan ZHOU, Chun-feng LIU   

  1. Zhenjiang First People's Hospital Zhenjiang First People's Hospital
  • Received:2009-11-03 Revised:2010-03-23 Online:2010-11-05 Published:2010-11-05
  • Contact: Xue-zhong LI,

摘要: 目的 研究脂多糖(LPS)对大鼠星形胶质细胞Toll样受体表达的影响及其机制。方法 在原代培养的第3代星形胶质细胞中加入不同浓度的LPS作用24h,通过免疫荧光、western blot观察星形胶质细胞 Toll样受体的表达和NF-κB p65的表达,同时研究NF-κB通路抑制剂对其的影响。结果 在正常状况下,星形胶质细胞胞浆和胞膜表达大量的TLR3受体,很少的TLR4受体。在LPS的刺激下,星形胶质细胞的TLR3表达保持不变,TLR4受体的表达随予以LPS的量增加而增高。LPS可刺激星形胶质细胞NF-κB的表达升高,抑制NF-κB通路活化抑制TLR4受体的上调。 结论 星形胶质细胞Toll样受体的表达是不同源的,TLR4受体随环境的变化而改变,其分子机制可能与NF-κB信号途径有关。

关键词: 脂多糖, 星形胶质细胞, TLR3, TLR4, NF-κB p65

Abstract: Objective To investigate the expression of toll-like receptors in astrocytes administrated with lipopolysaccharide (LPS). Methods LPS was administrated to rat astrocytes for 24h, and the expression of toll-like receptors and NF-κB p65 in astrocytes was detected by immunofluorescence and western blotting. At the same time, the effect of inhibitor of NF-κB signal pathway was investigated. Results Astrocytes expressed both cell surface and intracellular TLR3, low-level TLR4 in normal circumstance. LPS up-regulated the expression of TLR4 and NF-κB p65 in astrocytes in a concentration-dependent manner, while the expression of TLR3 kept constant. Pretreatment with SN90 (inhibitor of NF-κB) could block the increase of the expression of TLR4. Conclusion The expression of toll-like receptors in astrocytes was not homogeneous but rather tailored environmental signal. The molecular mechanism of the changes may be related to the expression of NF-κB p65.

Key words: lipopolysaccharide, astrocyte, TLR3, TLR4, NF-κB p65.