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吴煌1,李永忠1▲,李冬青2,陈亮3.IL-17RA特异性核酸适配子诱导实验性关节炎小鼠滑膜细胞分化方向的研究[J].中国医药科学,2024,14(11):13-16        基金项目:湖北省科技计划项目(2017CFB567)
IL-17RA特异性核酸适配子诱导实验性关节炎小鼠滑膜细胞分化方向的研究
Research on the differentiation direction of synovial cells induced by IL-17RA specific nucleic acid aptamer in experimental arthritis mice
  
DOI:
中文关键词:  适配子;白细胞介素-17受体A;白细胞介素-17;骨关节炎
英文关键词:Aptamer; Interleukin-17 receptor A; Interleukin-17; Osteoarthritis
作者单位
吴煌1,李永忠1▲,李冬青2,陈亮3 1.湖北省宜昌市第二人民医院 三峡大学附属第二人民医院骨外一科,湖北宜昌 443000; 2.武汉大学基础医学院,湖北武汉 430000;3.武汉大学人民医院运动医学科,湖北武汉 430072 
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中文摘要:
      [摘要] 目的 检测白细胞介素-17受体A(IL-17RA)特异性核酸适配子对实验性关节炎小鼠滑膜巨噬细胞(Mφ)和滑膜成纤维细胞(FLS)表型及功能的影响。 方法 手术切除小鼠膝关节内侧半月板,建立创伤性实验性关节炎的小鼠模型,检测IL-17RA特异性适配子RA10-6在体外对Mφ和FLS表型及功能的影响。结果 一定剂量的RA10-6作用小鼠滑膜巨噬细胞以后,可以升高细胞分化簇CD206分子表达水平,降低CD16/32分子水平,差异有统计学意义(P < 0.05);可促进巨噬细胞的人精氨酸酶1酶活性,同时对细胞诱导型一氧化氮合酶活性有一定的抑制作用;但是对CD163,树凝素-1分子影响不明显,差异无统计学意义(P > 0.05)。在RA10-6的作用下,小鼠滑膜巨噬细胞的白细胞介素-10显著增加,转化生长因子-β呈一定程度增加,但是增幅没有白细胞介素-10明显,而白细胞介素-12显著降低。RA10-6作用小鼠滑膜成纤维细胞以后,可以升高CD248分子表达水平,差异有统计学意义(P < 0.05),但是对CD90.5,血管细胞黏附分子-1影响不明显,差异无统计学意义(P > 0.05)。该适配子对细胞尿苷二磷酸葡糖脱氢酶活性无明显影响,差异无统计学意义(P > 0.05),但是对纤维连接蛋白的表达呈促进作用;在RA10-6的作用下,小鼠滑膜成纤维细胞的白细胞介素-6、 ? 趋化因子配体2、肿瘤坏死因子-α等细胞因子的影响差异无统计学意义(P > 0.05)。 结论 IL-17RA特异性适配子RA10-6通过诱导滑膜巨噬细胞表型改变,降低炎性细胞因子的表达,抑制关节炎的进程。
英文摘要:
      [Abstract] Objective To detect the impact of interleukin-17 receptor A (IL-17RA) specific nucleic acid aptamer on the phenotype and function of synovial macrophages (Mφ) and fibroblast-like synoviocytes (FLS) in experimental arthritis mice. Methods The medial meniscus of the knee joint in mice was surgically removed to establish a mouse model of traumatic experimental arthritis, and the impacts of IL-17RA specific nucleic acid aptamer RA10-6 on the phenotype and function of Mφ and FLS in vitro were detected. Results After a certain dose of RA10-6 was administered to mouse synovial Mφ, the expression level of CD206 molecules in cell differentiation clusters was increased, while the level of CD16/32 molecules was reduced, with statistically significant differences (P < 0.05). It could promote the enzymatic activity of human arginase-1 in Mφ and inhibit the activity of cell-inducible nitric oxide synthase to a certain extent. However, the impacts on CD163 and DECTIN-1 molecules were not obvious, without statistically significant differences (P > 0.05). Under the function of RA10-6, the levels of interleukin-10 in mouse synovial Mφ significantly increased. There was a certain degree of increase in transforming growth factor-β, but the increase was not as obvious as interleukin-10. Meanwhile, interleukin-12 was significantly reduced. After RA10-6 acted on mouse synovial fibroblasts, the expression level of CD248 molecule could be increased, with statistically significant differences (P < 0.05). However, the impact on CD90.5 and vascular cell adhesion molecule-1 was not obvious, without statistically significant differences (P > 0.05). The aptamer had no obvious impact on the activity of cell uridine diphosphate glucose dehydrogenase, without statistically significant difference (P > 0.05). However, it had a promoting function on the expression of fibronectin. Under the function of RA10-6, there were no statistically significant differences in the impacts of cytokines such as interleukin-6, chemokine ligand 2 and tumor necrosis factor-α on mouse synovial fibroblasts (P > 0.05). Conclusion IL-17RA specific nucleic acid aptamer RA10-6 can reduce the expression of inflammatory cytokines and inhibit the progress of arthritis by inducing phenotypic changes of synovial Mφ.
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