首页> 中文期刊>中国循证心血管医学杂志 >曲格列酮分化调节人单核细胞源性巨噬细胞Kv1.3和Kir2.1表达及其对膜电位的影响

曲格列酮分化调节人单核细胞源性巨噬细胞Kv1.3和Kir2.1表达及其对膜电位的影响

     

摘要

目的 研究曲格列酮对人单核细胞源性巨噬细胞电压依赖性钾通道Kv1.3、内向整流钾通道Kir2.1表达及膜电位的影响.方法 以健康人外周血单核细胞源性巨噬细胞为研究对象,采用Real time RT-PCR及Western blot技术观察曲格列酮对巨噬细胞Kv1.3、Kir2.1表达的调节作用和电压敏感染料膜电位标测技术分析其对巨噬细胞膜电位的影响.结果 50 μmol/L曲格列酮显著抑制巨噬细胞Kv1.3的表达,mRNA和蛋白表达下降分别超过82%和60%(P<0.05),而对Kir2.1的表达没有明显影响(P>0.05);同时,巨噬细胞膜电位下降了约23%(P<0.05).结论 曲格列酮分化调节人单核细胞源性巨噬细胞Kv1.3和Kir2.1表达,降低巨噬细胞膜电位.%Objective To study the influences of troglitazone on the expressions of Kvl. 3 ,Kir2. 1 and membrane potential in human monocyte-derived macrophages. Methods Taking monocyte-derived macrophages in peripheral blood of health people as objects, the regulation effects of troglitazone on the expressions of Kvl. 3 and Kir2. 1 were observed by using RT-PCR and Western-blot method. The influence of troglitazone on macrophage membrane potential was analyzed by using optical mapping of the membrane potential with voltage-sensitive dyes. Results Troglitazone ( 50 μmol/L ) inhibited significantly the expression of Kv1. 3, and the mRNA expression and protein expression of Kvl. 3 decreased over 82% and 60% respectively ( P < 0. 05 ), and it had no significant influence on Kir2. 1 ( P > 0. 05 ). At the same time macrophage membrane potential reduced about 23% ( P <0.05 ). Conclusion Troglitazone can regulate differentially the expressions of Kv1. 3 and Kir2. 1 and reduce membrane potential in human monocyte-derived macrophages.

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