Interleukin-5 (IL-5) is manifested as its involvement in the process of atherosclerosis, but the mechanism is still unknown. In this study, we explored the effect of IL-5 on lipid metabolism and its underlying mechanisms in THP-1-derived macrophages. The quantitative polymerase chain reaction (qPCR) and western blot analysis results showed that IL-5 significantly up-regulated ATP-binding cassette transporter A1 (ABCA1) expression in a dose-dependent and time-dependent manner. [³H]-labeled cholesterol was used to assess the levels of cholesterol efflux, and the results showed that IL-5 increased ABCA1-mediated cholesterol efflux. A high-performance liquid chromatography assay indicated that cellular cholesterol content was decreased by IL-5 treatment in THP-1-derived macrophages. The selective inhibitor and small interfering RNA were used to block the Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway. The results of the qPCR and western blot analysis showed that IL-5 activated JAK2/STAT3 pathway to up-regulate ABCA1 expression. Meanwhile, IL-5 reduced the expression level of miR-211. Furthermore, we found that JAK2 is a target gene of miR-211 and miR-211 mimic inhibited the expression of JAK2 and reduced the levels of p-STAT3 and ABCA1 as revealed by luciferase reporter assay, qPCR and western blot analysis. In summary, these findings indicated that IL-5 promotes ABCA1 expression and cholesterol efflux through the miR-211/JAK2/STAT3 signaling pathway in THP-1-derived macrophages.

中文翻译：

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Interleukin-5通过THP-1衍生的巨噬细胞中的miR-211 / JAK2 / STAT3途径促进ATP结合盒转运蛋白A1的表达。

白介素5（IL-5）表现为参与动脉粥样硬化的过程，但其机制仍不清楚。在这项研究中，我们探讨了IL-5对THP-1衍生的巨噬细胞中脂质代谢的影响及其潜在机制。定量聚合酶链反应（qPCR）和蛋白质印迹分析结果表明，IL-5以剂量依赖性和时间依赖性方式显着上调了ATP结合盒转运蛋白A1（ABCA1）的表达。[ ³H 1标记的胆固醇用于评估胆固醇外排水平，结果表明IL-5增加了ABCA1介导的胆固醇外排。高效液相色谱分析表明，IL-5处理可降低THP-1衍生的巨噬细胞中细胞胆固醇的含量。使用选择性抑制剂和小干扰RNA来阻断Janus激酶（JAK）/信号转导子和转录激活因子3（STAT3）通路。qPCR和蛋白质印迹分析的结果表明，IL-5激活了JAK2 / STAT3途径来上调ABCA1表达。同时，IL-5降低了miR-211的表达水平。此外，我们发现JAK2是miR-211的靶基因，而miR-211模拟物可抑制JAK2的表达并降低p-STAT3和ABCA1的水平，qPCR和蛋白质印迹分析。总之，这些发现表明IL-5通过THP-1衍生的巨噬细胞中的miR-211 / JAK2 / STAT3信号通路促进ABCA1表达和胆固醇外排。