摘要
目的观察载脂蛋白A1对骨髓源性巨噬细胞极性的影响,探讨高密度脂蛋白抗炎的细胞机制。方法体外培养小鼠骨髓源性巨噬细胞,分别用5、10、15 mg/L浓度的载脂蛋白A1孵育细胞24 h后,应用流式细胞术检测膜分子CD16/32、CD206的表达;用酶联免疫吸附法检测白细胞介素10和白细胞介素12的分泌;用实时荧光定量聚合酶链反应检测Toll样受体4、髓样分化因子88、干扰素调节因子5 mRNA的表达。结果经载脂蛋白A1干预后的巨噬细胞,CD16/32、白细胞介素12表达明显下降,CD206、白细胞介素10表达明显升高,并伴有Toll样受体4、髓样分化因子88、干扰素调节因子5 mRNA表达的下降,呈剂量依赖性。结论载脂蛋白A1促进巨噬细胞向抗炎性M2型巨噬细胞极化,此效应可能与高密度脂蛋白的抗炎作用有关。
Aim To explore the anti-inflammatory mechanisms of high density lipoprotein （HDL） by observing the effects of apolipoprotein A1 （ApoA1）,a major protein component of HDL,on the mouse bone barrow macrophage polarity. Methods Apo A1 （5,10,15 mg/L） were added to the cultured mice marrow-derived macrophages for 24 h.The expression of membrane molecules CD16/32,CD206 were detected using fluorescence activated cell sorting （FACS） Enzyme-linked immunosorbent assay （ELISA） were used to detect the secretion of interleukin-10 （IL-10） and IL-12 Real-time quantitative polymerase chain reaction were used to detect the expression of Toll like receptor 4 （TLR4）,myeloid differentiation factor 88 （MyD88）,interferon regulatory factor 5 （IRF5） mRNA. Results After incubation mice marrow-derived macrophage with ApoA1 （5,10,15 mg/L） for 24 h,the expression of CD16/32,IL-12 was decreased,expression of CD206,IL-10 expression was elevated,and the expression of TLR4,MyD88,IRF5 mRNA was decreased.Conclusion ApoA1 promote macrophages towards an anti-inflammatory M2 phenotype,which may be responsible for the anti-inflammatory effects of HDL.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2013年第10期865-870,共6页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金(81160028)
广西卫生厅重点课题(重2012006
重200979)
2009年广西教育厅科研资助项目(200911LX293)
2009年度留学回国人员科技活动资助项目(200914)
关键词
载脂蛋白A1
巨噬细胞极性
抗炎
APOA1 promote macrophages towards an anti-inflammatory M2 phenotype, which may be responsible for theanti-inflammatory effects of HDL.
