Rheumatoid arthritis is a chronic systemic autoimmune disease. In this study, the role of microRNA-340-5p in rheumatoid arthritis was investigated. qRT-PCR was used to detect the expression of microRNA-340-5p in serums, synovial tissues, and fibroblast-like synoviocytes from patients and healthy participants. Cell proliferation rate, cell cycle and apoptotic cell numbers were measured by CCK-8 and flow cytometry assays. The expression of pro-inflammation factors was determined by ELISA. Our data showed that the expression of microRNA-340-5p was greatly suppressed in rheumatoid arthritis serums, synovial tissues and rheumatoid arthritis-fibroblast-like synoviocytes compared to that in healthy controls. Over-expression of microRNA-340-5p greatly suppressed cell proliferation, promoted cell apoptosis, and suppressed the expression of inflammation factors in rheumatoid arthritis fibroblast-like synoviocytes. Additionally, STAT3 was a target of microRNA-340-5. Overexpression of STAT3 could reverse the outcome of microRNA-340-5p on cell proliferation and apoptosis in rheumatoid arthritis fibroblast-like synoviocytes. The findings in our study demonstrated that microRNA-340-5p may serve as a potential target for therapeutic direction for patients with rheumatoid arthritis.

类风湿关节炎是一种慢性全身性自身免疫性疾病。在这项研究中，研究了microRNA-340-5p在类风湿关节炎中的作用。使用qRT-PCR检测来自患者和健康受试者的血清，滑膜组织和成纤维样滑膜细胞中microRNA-340-5p的表达。通过CCK-8和流式细胞术测定细胞增殖率，细胞周期和凋亡细胞数。通过ELISA测定促炎因子的表达。我们的数据显示，与健康对照组相比，类风湿关节炎血清，滑膜组织和类风湿关节炎成纤维细胞样滑膜细胞中microRNA-340-5p的表达受到极大抑制。microRNA-340-5p的过度表达可大大抑制细胞增殖，促进细胞凋亡，并抑制了类风湿关节炎成纤维样滑膜细胞中炎症因子的表达。另外，STAT3是microRNA-340-5的靶标。STAT3的过表达可以逆转microRNA-340-5p对类风湿关节炎成纤维细胞样滑膜细胞增殖和凋亡的影响。我们研究中的发现表明，microRNA-340-5p可以作为类风湿关节炎患者治疗方向的潜在靶标。