中文摘要：

肥胖进程中，脂肪组织中的巨噬细胞由抗炎性的M2（2型巨噬细胞）逐渐极化成促炎性的M1（1型巨噬细胞），M1分泌的促炎性细胞直接可以导致胰岛素抵抗等肥胖相关代谢综合症。由于体外常用细菌脂多糖（Lipopolysaccharide，LPS）诱导的促炎性巨噬细胞来研究脂肪组织中巨噬细胞的极化，但其与脂肪组织中M1的表型相差甚远；另外，粒细胞-巨噬细胞集落刺激因子（granulocyte-rnacrophage colony stimulating fac—tor，GIcsF）和巨噬细胞集落刺激因子（macrophage colony stimulating factor，M-CSF）可以诱导骨髓细胞分化为骨髓来源巨噬细胞（bone marrow-derived macrophage，BMDM）。文章发现GM-CSF诱导的巨噬细胞（GM-CSF-induced macrophages，GIVI-BMM）高表达脂肪组织M1型标志基因CDllc与NOS2和促炎性细胞因子IL6与TNFa；与此相反，M-CSF诱导的骨髓细胞分化的巨噬细胞（M-CSF-induced macrophages，M-BMM）高表达脂肪组织M2标志基因CD206和抗炎性细胞因子／L10。因此，GM-BMM和M-BMM更适合用于脂肪组织巨噬细胞极化的体外研究。

英文摘要：

In the process of obesity, macrophages polarize from anti-inflammatory M2 to pro-inflamma-tory M1 in adipose tissues. Inflammatory cells secreted from M1 can induce insulin resistance and obe-sity related metabolic syndrome directly. Lipopolysaccharide（LPS） is often used to induce pro-inflam-matory macrophages to study macrophages polarization in adipose tissues in vitro. However, LPS-in-duced macrophages are drastically different from M1 in adipose tissues. Furthermore, granulocyte-macrophage colony stimulating factor （GM-CSF） and macrophage colony stimulating factor （M-CSF）can induce bone marrow into bone marrow-derived macrophage（BMDM）. It was found that GM-CSF-induced macrophages（GM-BMM） could strongly express adipose tissues related M1 markers genesCDllc and NOS2 and inflammatory cytokines IL6 and TNFa. On the contrary, M-CSF-induced mac-rophages（M-BMM） could highly express adipose tissues related M2 markers genes CD206 and anti-in-flammatory cytokines ILIO. Consequently, GM-BMM and M-BMM are more suitable for adipose tis-sues related macrophages polarization in vitro.