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目的 研究Zeste基因增强子人类同源物2(EZH2)抑制剂GSK343调节巨噬细胞亚群的分化,探讨EZH2在牙周炎中潜在的治疗作用.方法 将巨噬细胞RAW264.7分为4组:空白组(A组)、对照组(B组)、内毒素(LPS)刺激组(C组)、LPS+GSK343组(D组).细胞经培养及相应处理后,利用免疫印迹和酶联免疫吸附试验检测其表型生物学标志变化,包括肿瘤坏死因子-α(TNF-α)、诱导型一氧化氮合酶(iNOS)、白细胞介素-10(IL-10)和精氨酸酶-1(Arg-1).利用大肠杆菌吞噬试验检测巨噬细胞RAW264.7在不同条件下对大肠杆菌的吞噬作用.结果LPS可以诱导RAW264.7产生M1表型生物标志(TNF-α和iNOS表达增加),在加入EZH2抑制GSK343后,IL-10和Arg-1表达升高,提示EZH2抑制剂GSK343可以诱导RAW264.7细胞由M1型向M2型转化;RAW264.7细胞具有吞噬大肠杆菌的作用,加入LPS的条件下吞噬大肠杆菌作用加强,而EZH2抑制剂GSK343可以调节RAW264.7细胞对大肠杆菌的吞噬作用.结论 EZH2抑制剂GSK343可以调节巨噬细胞的分化,在牙周炎的治疗中可能具有潜在作用.“,”ObjectiveTo explore the therapeutic effect of enhancer of Zeste homolog 2 (EZH2) inhibitor GSK343 on periodontitis by regulating microphage differentiation.Methods Macrophage RAW264.7 cells were divided into the blank (A group), control (B group), lipopolysaccharide (LPS) stimulation (C group), and LPS+GSK343 (D group) groups. Phenotype transformations was determined through Western blot analysis and enzyme-linked immunosorbent assay by detecting the differentiation of phenotypic biological markers, including tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), interleukin-10 (IL-10), and Arginase-1 (Arg-1). Metergasis was identified by performing a phagocytosis test onEsche-richia coli (E. coli).Results Macrophage RAW264.7 cells produced classical phenotypic biomarkers (M1) TNF-α and iNOS under LPS stimulation. The expression levels of IL-10 and Arg-1 increased after adding GSK343 into the culture medium. GSK343 also induced the conversion of M1 macrophages into M2 macrophages. Macrophage RAW264.7 cells exerted a phagocytic effect onE. coli, and this effect was enhanced after adding LPS into the culture medium. GSK343 regulated the macrophage RAW264.7 phagocytosis ofE. coli.Conclusion GSK343 possibly participates in the regulation of macrophage differentiation and, consequently, in the latent treatment of periodontitis.