Aβ1-42通过TLR4影响小鼠巨噬细胞RAW264.7炎症因子IL-1β和IL-6释放

The effect of Aβ1-42 on the release of RAW264.7 inflammatory cytokines IL-1β and IL-6 in murine macrophages via TLR4

目的探讨Aβ1-42对小鼠巨噬细胞RAW264.7向炎症性细胞转变的影响及机制。方法 RAW264.7细胞分别经过LPS与Aβ1-42刺激,RT-PCR和Western blot检测GM-CSF受体CSF2RA和CSF2RB的表达水平,ELISA检测在Aβ1-42刺激下的炎症因子IL-1β、IL-6和TNF-α水平;采用TLR4抑制剂分别干预LPS和Aβ1-42处理后的RAW264.7,检测CSF2RA与CSF2RB受体的表达变化,炎症因子IL-1β、IL-6的释放。结果 RAW264.7细胞表面GM-CSF受体CSF2RB在LPS与Aβ1-42处理后表达水平均比对照组升高(P<0.05),而CSF2RA表达没有显著性改变;炎症因子IL-6与IL-1β在Aβ1-42刺激后分泌增加,同时TLR4抑制剂抑制LPS和Aβ1-42对细胞的刺激。结论 Aβ1-42通过TLR4促进小鼠RAW264.7细胞炎症因子IL-6、IL-1β的分泌。

Objective To investigate the effect and mechanism of Aβ1-42 on the transformation of mouse macrophages RAW264.7 to inflammatory cells.Methods RAW264.7 cells were stimulated by LPS and Aβ1-42 pretreated with or without TLR4 inhibitor,then the expressions of GM-CSF receptor CSF2 RA and CSF2 RB were detected by RT-PCR and Western blot,and the levels of inflammatory factors IL-1β,IL-6 and TNF-αwere detected by ELISA.Results The expression level of GM-CSF receptor CSF2 RB on the surface of RAW264.7 cells increased after LPS and Aβ1-42 treatment(P<0.05),compared to normal control.LPS and Aβ1-42 stimulated the increased secretion of IL-6 and IL-1β,but inhibited by TLR4 inhibitor.Conclusion Aβ1-42 promotes the secretion of IL-6,IL-1βin RAW264.7 cells via TLR4.