脂氧素A_4抑制单核巨噬细胞源性树突状细胞的分化及成熟

Lipoxin A4 Inhibits Lipopolysaccharide-induced Differentiation of RAW264.7 Murine Macrophages into Dendritic-like Cells and Its Maturation

目的探讨内源性抗炎症脂质介质脂氧素A4对巨噬细胞向树突状细胞分化及树突状细胞成熟的影响。方法体外培养小鼠巨噬细胞(RAW264.7细胞),根据分组,分别以0μg/L(对照组)、100μg/L的脂多糖、100μg/L的脂多糖联合100 nmol/L或500 nmol/L的脂氧素A4干预小鼠单核巨噬细胞48 h,以流式细胞仪测定细胞表面标记物MHC-II、CD80及CD86的表达,并以激光共聚焦显微镜及相差显微镜观察细胞形态。结果脂氧素A4能显著减少脂多糖刺激下RAW264.7细胞向树突状细胞的转化,并抑制脂多糖刺激下RAW264.7细胞MHC-II及CD86的表达(P<0.01),而对CD80表达无明显影响(P>0.05)。结论脂氧素A4能抑制脂多糖刺激的小鼠巨噬细胞向树突状细胞转化及成熟,可能通过负向调控免疫炎症反而抑制动脉粥样硬化。

Aim To investigate the effects of lipoxin A4 （LXA4 ） on lipopolysaccharide （LPS）-induced differentiation and mature of RAW264. 7 macrophages into dendritic like cells （DC）. Methods RAW264. 7 murine macrophages were respectively treated with LPS （0 μg/L and 100 μg/L）, LPS （100 μg/L） together with LXA4 （100 nmol/L and 500 nmol/L）. Cells surface markers （CD80, CD86 and MHC-II） were analyzed by FACS, and cell morphology was observed by laser scanning confoeal microscope and phase contrast microscope. Results LPS could significantly pro- mote the differentiation of RAW264. 7 murine macrophages into DC and the expression of surface molecules （ CD80, CD86, MHC-II） （P 〈0. 01 ）, and LXA4 could inhibit the differentiation of LPS-stimulated RAW264. 7 murine macrophages and down-regulate the expression of CD86 and MHC-II, but had no significant effect on the expression of CD80. Conclusion LXA4 could negatively regulate the differentiation of RAW264. 7 into DC and inhibit the maturation of DC, which may inhibit the pathogenesis and development of atherosclerosis by negatively regulating immuno-inflammatory response.