【摘要】 目的:探讨血管紧张素Ⅱ（AngⅡ）是否能通过核因子-κB（NF-κB）途径调节巨噬细胞移动抑制因子（MIF）的表达。方法:佛波酯诱导THP-1细胞48 h使其转化为巨噬细胞。第一组:对照组:AngⅡ1×10^-8mol/L组;AngⅡ1×10^-7mol/L组;AngⅡ1×10^-6mol/L组;AngⅡ1×10^-5mol/L组。第二组:对照组;AngⅡ1×10^-6mol/L组:AngⅡ1×10^-6mol/L+PDTC组:PDTC组。Western blot检测第一组细胞核内NF-κB的表达。Real time RT-PCR检测第二组巨噬细胞MIF mRNA的表达。ELISA检测第二组巨噬细胞上清液中MIF的含量。结果:Western Blot:随着AngⅡ浓度的增高,NF-κBp65的表达逐渐增强。Real time RT-PCR:AngⅡ组MIF mRNA表达量明显高于对照组:PDTC作用后,由AngⅡ诱导的MIF mRNA表达明显降低。ELISA:AngⅡ组MIF含量明显高于对照组;PDTC作用后,由AngⅡ诱导增加的MIF含量明显降低。结论:AngⅡ能通过NF-κB信号通路促进巨噬细胞MIF mRNA的表达和MIF的分泌。更多还原

【Abstract】 Objective To investigate whether angiotensin Ⅱ(AngⅡ) can regulate the expression of MIF in macrophages via the NF-κB pathway. Methods Western Blot, real time RT-PCR and ELISA were used in the present study. Results Western blot result showed that the expression of NF-κBp65 gradually increased with the increase of the concentration of Ang Ⅱ. Results of real time RT-PCR and ELISA revealed that MIF m RNA expression and the content of MIF were significantly higher in Ang Ⅱ group than those in the control group. PDTC could reverse the effect of Ang Ⅱ on MIF m RNA expression and MIF secretion in macrophages.Conclusion Ang Ⅱ can promote MIF m RNA expression and MIF secretion in macrophages via the NF-κB signaling pathway.更多还原