中文摘要：

目的考察黑种草子中的活性成分百里醌（thymoquinone）对M2型巨噬细胞极化的调控机制。方法利用白介素4（IL-4）诱导鼠源巨噬细胞为M2型巨噬细胞模型;MTT法观察百里醌对细胞活力的影响;Trans-well小室迁移实验考察巨噬细胞造模前后自身迁移力的变化、对乳腺癌4T1细胞的迁移能力变化及百里醌干预的影响;qRT-PCR法考察百里醌对M2型巨噬细胞内精氨酸酶1（Arg1）、诱导型一氧化氮合酶（iNOS）m RNA的影响;Western blot法考察百里醌对细胞内ARG1、i NOS蛋白及信号传导与转录激活因子6（STAT6）信号通路的影响。结果百里醌不仅抑制巨噬细胞向M2表型极化后自身迁移力的提高,也抑制M2型巨噬细胞促进乳腺癌4T1细胞的体外迁移加剧。百里醌呈剂量依赖性抑制Arg1同时提高i NOS的表达,降低STAT6蛋白的磷酸化水平。结论百里醌逆转巨噬细胞M2表型极化,部分通过抑制IL-4/STAT6信号通路的活化,调控Arg1/iNOS的表达消长而干预M2表型极化进程中巨噬细胞自身及其促乳腺癌细胞的体外迁移加速。

英文摘要：

AIM To study the mechanism of thymoquinone from Semen Nigellae on its regulation of M2 phenotype polarization of macrophages in vitro. METHODS IL-4（ 60 ng / m L） induced RAW264. 7 cells to establish the M2 macrophage model. MTT assay was used to measure the cell cytotoxicity of thymoquinone. Trans-well assay was used for measurement of migration capability; q RT-PCR was used to determine m RNA expression of Arg1 and i NOS. Western blot was used for protein expressions of ARG1,iNOS and phosphorylation of STAT6. RESULTS Thymoquinone not only inhibited the increased migratory capability of macrophage towards M2 phenotype,but also repressed breast cancer cells migration with the aid of M2 macrophages in vitro. Thymoquinone down-regulated the gene and protein expression of Arg1 while up-regulated the gene and protein expression of iNOS,and suppressed the phosphorylation of STAT6 protein. CONCLUSION Thymoquinone can reverse macrophage polarization from M2 to M1 phenotype and inhibits the promotion of M2 macrophages to breast cancer cells migration in vitro. IL-4 /STAT6 signal pathway is partly involved to regulate the expression between Arg1 and iNOS under the interference of thymoquinone.