目的探讨常山酮(HF)对小鼠子宫内膜异位症(EMs)中巨噬细胞极化的调控作用。方法构建EMs小鼠模型,观察并计算小鼠异位灶体积。流式细胞术检测巨噬细胞标志物,包括M1型(CD16/32~+,CD197~+)和M2型(CD206~+,CD14~+);Western blotting检测巨噬细胞标志蛋白,包括M1型(i NOS,IL-12)和M2型(Arg-1,IL-10)的表达;ELISA检测各炎症因子水平,最后TGF-β1诱导单独分离的巨噬细胞,Western blotting和流式细胞术分别检测i NOS和Arg-1的表达及阳性细胞数目。结果 HF抑制EMs鼠异位内膜的体积增加;使M1型细胞数目增加,M2减少;M1型标志蛋白的表达增加,M2降低;促炎因子含量升高,抑炎因子含量降低;HF使TGF-β1诱导的巨噬细胞中i NOS~+细胞数目增加,IL-10~+减少。结论 HF可直接作用于巨噬细胞,维持EMs模型鼠炎症微环境的平衡,抑制巨噬细胞向M2型极化,减少EMs鼠异位内膜体积。 Aim To investigate the regulation of macrophage polarization by albuterol (HF) in mouse endometriosis (EMs). Methods The mouse model of EMs was constructed and the volume of heterotopic foci in mice was observed and calculated. Flow cytometry was used to detect macrophage markers including M1 (CD16 / 32 ~ +, CD197 ~ +) and M2 (CD206 ~ +, CD14 ~ +); macrophage marker proteins including M1 (iNOS, IL-12) and M2 (Arg-1, IL-10). ELISA was used to detect the levels of inflammatory cytokines. Finally, macrophages isolated by TGF-β1 were induced by Western blotting and flow cytometry The expression of iNOS and Arg-1 and the number of positive cells were detected. Results HF inhibited the increase of ectopic endometrium in EMs rats, increased the number of M1 cells and M2, decreased the expression of M1 marker and M2, decreased the levels of proinflammatory cytokines and anti-inflammatory cytokines, The number of iNOS ~ + cells in the -β1-induced macrophages increased and IL-10 ~ + decreased. Conclusion HF can directly act on macrophages and maintain the balance of inflammation microenvironment in EMs model mice, inhibit the polarization of macrophages to M2 type, and decrease the volume of ectopic endometrium in EMs mice.