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作 者:张红[1] 李学忠[1] 白龙梅[2] 杨亚萍[2] 周媛[2] 刘春风[2]
机构地区:[1]镇江市第一人民医院神经科,江苏镇江212005 [2]苏州大学衰老和神经疾病实验室,江苏苏州215004
出 处:《基础医学与临床》2010年第11期1206-1209,共4页Basic and Clinical Medicine
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24 h,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,星形胶质细胞在胞质和胞膜表达大量的TLR3受体及很少的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LPS量的增加而增高。LPS可刺激星形胶质细胞NF-κB的表达升高,抑制NF-κB通路活化可抑制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。Objective To investigate the expression of toll-like receptors in astrocytes administrated with lipopolysaccharide(LPS).Methods LPS was administrated to rat astrocytes for 24 h,and the expression of toll-like receptors and NF-κB P65 in astrocytes was detected by immunofluorescence and Western blot.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 SN50(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.
关 键 词:脂多糖 星形胶质细胞 TLR3 TLR4 NF-ΚB P65
分 类 号:R741.02[医药卫生—神经病学与精神病学]
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