Molecular Analysis of Curcumin-induced Polarization of Murine RAW264.7 Macrophages
Molecular Analysis of Curcumin-induced Polarization of Murine RAW264.7 Macrophages
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姜黄素诱导的小鼠 RAW264.7 巨噬细胞极化的分子分析
DOI：
10.1097/fjc.0000000000000079
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发表时间：
2014-06-01
影响因子：
3
通讯作者：
Yuan, Zuyi
中科院分区：
文献类型：
--
作者：
Chen, Fangyuan;Guo, Ning;Yuan, Zuyi
摘要：本研究旨在研究姜黄素对巨噬细胞极化的影响及其可能的机制，并分析其抗动脉粥样硬化作用的分子基础。用姜黄素处理RAW264.7巨噬细胞(M0)和M_1巨噬细胞(M_1)，观察姜黄素在0、6.25、12.5和25℃摩尔/L浓度下加或不加GW9662。采用实时定量聚合酶链式反应和Western印迹分析方法，检测巨噬细胞M1[iNOS、IL-1、IL-6、MCP-1]和M2(KLF4、FIZZ1、MGL1)的表型标志物。姜黄素降低M0和M1巨噬细胞的M1表型标志物的表达，上调M0和M1巨噬细胞的增殖激活受体和M1巨噬细胞的Ikb和agr；的表达。当姜黄素和GW9662与M1巨噬细胞共同孵育时，M1表型标志物的表达降低，而IkB和agr；上调。姜黄素作用后，M0和M1巨噬细胞M2表型标志物的表达上调。当M0和M1巨噬细胞与姜黄素和GW9662共同孵育时，M2表型标志物的表达减少。姜黄素通过直接激活IkB和agr；抑制M1炎症表型，并通过激活增殖物激活受体ggr；使巨噬细胞极化为M2表型。这些发现为开发治疗动脉粥样硬化的新药提供了新的线索。
Abstract: This study aimed to investigate the effects of curcumin on macrophages polarization and possible mechanism involved, and to analyze the molecular basis of its antiatherosclerosis activity. RAW264.7 macrophages (M0) and M1 macrophages were treated with curcumin at 0, 6.25, 12.5, and 25 &mgr;mol/L with or without GW9662. Using real-time polymerase chain reaction and Western blot analysis, we examined the phenotype markers of M1 [iNOS, interleukin (IL)-1&bgr;, IL-6, and MCP-1] and M2 (KLF4, FIZZ1, and MGL1] macrophages. Curcumin reduced the expression of the M1 phenotype markers and upregulated the expression of proliferator-activated receptor &ggr; in M0 and M1 macrophages and IKB&agr; in M1 macrophages. When M1 macrophages were incubated with curcumin and GW9662, the expression of the M1 phenotype markers was decreased, while IKB&agr; was upregulated. The expression of the M2 phenotype markers in M0 and M1 macrophages was upregulated after the curcumin treatment. When M0 and M1 macrophages were incubated with curcumin and GW9662, the expression of the M2 phenotype markers was reduced. Curcumin inhibited the M1 inflammation phenotype as a result of the direct activation of IKB&agr; and polarized the macrophages to become M2 phenotype through the activation of proliferator-activated receptor &ggr;. These findings provide new clues to develop new drug therapy for atherosclerosis.