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作 者:陈方圆[1] 袁祖贻[1] 周娟[1] 王欢[1] 薛丽[2] 郭宁[1]
机构地区:[1]西安交通大学医学部第一附属医院心血管病医院,陕西西安710061 [2]西安交通大学医学部免疫学与病原微生物学教研室,陕西西安710061
出 处:《西安交通大学学报(医学版)》2015年第2期257-262,共6页Journal of Xi’an Jiaotong University(Medical Sciences)
基 金:国家自然科学基金面上项目(No.18110221)~~
摘 要:目的观察姜黄素对LPS和IFNγ诱导的RAW264.7巨噬细胞(M1)极化的影响及机制。方法不同浓度姜黄素(6.25、12.5、25μmol/L)干预LPS和IFNγ诱导的RAW264.7巨噬细胞(M1)12h,同时再加入20μmol/L GW9662与25μmol/L姜黄素共同干预LPS和IFNγ诱导的RAW264.7巨噬细胞(M1)12h,采用Real-time PCR、ELISA及Western blot方法检测IL-1β、IL-6和M2表型标志分子KLF4、FIZZ1、MGL1、PPARγ的表达,及阻断PPARγ后KLF4和FIZZ1的表达。结果不同浓度姜黄素均能上调LPS和IFNγ诱导的RAW264.7巨噬细胞(M1)的M2标志分子的表达,并且抑制炎症因子IL-1β和IL-6的分泌;阻断PPARγ后,RAW264.7巨噬细胞源性M1表型巨噬细胞表达M2标志分子下调。结论姜黄素通过活化PPARγ促进LPS和IFNγ诱导的RAW264.7巨噬细胞(M1)向M2表型极化。Objective To observe the effect of curcumin on RAW264.7 macrophages induced with LPS and IFNγ(M1)and the mechanisms involved.Methods Curcumin of different concentrations (6.25 μmol/L,12.5μmol/L and 25 μmol/L)was used to treat RAW264.7 macrophages induced with LPS and IFNγ(M1)for 12 h,and RAW264.7 macrophages induced with LPS and IFNγ(M1)were incubated with 20μmol/L GW9662 and 25 μmol/L curcumin for 12 h.Using Real-time PCR,ELISA and Western blotting analysis,we examined the expressions of IL-1β,IL-6,PPARγand phenotype markers M2 (KLF4,FIZZ1,and MGL1 )and the expressions of KLF4 and FIZZ1 when PPARγwas inhibited.Results Curcumin of different concentrations all could inhibit the expressions of IL-1βand IL-6 in RAW264.7 macrophages induced with LPS and IFNγ(M1).Curcumin of different concentra-tions could upregulate the expression of M2 markers (KLF4,FIZZ1 and MGL1)and PPARγin RAW264.7 macro-phages induced with LPS and IFNγ(M1).When M1 macrophages were incubated with curcumin and GW9662,the expression of the M2 phenotype markers was reduced.Conclusion Curcumin polarized the M1 phenotype macro-phages derived from RAW264.7 macrophages to become M2 phenotype through activating PPARγ.
关 键 词:姜黄素 RAW264.7巨噬细胞 巨噬细胞极化 M1/M2表型 过氧化物酶体增殖激活物受体y(PPARy) 脂多糖 y干扰素
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