山东大学学报 (医学版) ›› 2025, Vol. 63 ›› Issue (12): 74-78.doi: 10.6040/j.issn.1671-7554.0.2025.0692
• 临床医学 • 上一篇
宋慧梳1,孙志坚2,张邱婷1,弭雪1,张妮1,王志仑1,尹哲1,郝学喜1,王迎雪1
SONG Huishu1, SUN Zhijian2, ZHANG Qiuting1, MI Xue1, ZHANG Ni1, WANG Zhilun1, YIN Zhe1, HAO Xuexi1, WANG Yingxue1
摘要: 目的 探讨miR-125a-3p对类风湿关节炎滑膜成纤维细胞(rheumatoid arthritis synovial fibroblasts, RA-FLS)增殖能力及炎症因子分泌水平的影响。 方法 选取类风湿关节炎(rheumatoid arthritis, RA)患者25例,无菌获得其关节置换术后的滑膜组织,分离出RA-FLS用于实验研究。通过细胞转染将miR-125a-3p mimics及miR-NC转染到RA-FLS中进行细胞培养,将培养细胞分为Control组、miR-NC组及miR-125a-3p mimics组,实时定量PCR(real-time quantitative PCR,RT-qPCR)法检测各组细胞中miR-125a-3p的表达,细胞计数试剂盒-8(cell-counting-kit-8, CCK-8)测定细胞增殖能力,酶联免疫吸附试验(enzyme linked immunosorbent assay, ELISA)检测细胞培养上清液中肿瘤坏死因子α(tumor necrosis factor α,TNF-α)、白细胞介素-6(interleukin-6, IL-6)和白细胞介素-1β(interleukin-1β, IL-1β)的水平。 结果 miR-125a-3p mimics组RA-FLS的细胞活力以及细胞培养上清液中TNF-a、IL-1β和IL-6的水平较miR-NC组下降,差异有统计学意义(P<0.001)。 结论 miR-125a-3p抑制RA-FLS增殖及炎症因子的分泌,可能成为研究RA发病机制的新靶点。
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