LncRNA OIP5-AS1在多种癌症和肿瘤中普遍存在基因失衡，这在调控其生物学功能中发挥着重要作用。然而，在类风湿关节炎（RA）中，对LncRNA OIP5-AS1的研究还很少。本研究旨在探讨LncRNA OIP5-AS1在RA发病机制中的作用。在本研究中，我们建立了佐剂性关节炎（AA）大鼠模型，获得原代纤维样滑膜细胞（FLSs）；通过荧光原位杂交（FISH）检测了LncRNA OIP5-AS1基因的亚细胞定位；通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴化物（MTT）检测，确定了FLSs的细胞增殖；通过酶联免疫吸附法（ELISA）测定了IL-1β、IL-6和TNF-α的浓度；采用定量实时PCR（qRT-PCR）、Western blot（WB）和免疫荧光检测了FLSs中LncRNA OIP5-AS1 / miR-410-3p / wnt7b信号通路和Wnt / β- 肌动蛋白信号通路相关指标的表达。 FISH检测证实LncRNA OIP5-AS1存在于细胞质中，表明其作为竞争性内源性RNA（ceRNA）发挥作用。qRT-PCR显示FLSs中LncRNA OIP5-AS1的表达上调，而miR-410-3p的表达下调。我们还发现，LncRNA OIP5-AS1沉默抑制了FLSs的增殖和炎症反应。此外，miR-410-3p的下游靶基因Wnt7b的表达以及Wnt / β-肌动蛋白信号通路的激活也受到了LncRNA OIP5-AS1沉默的抑制。这些结果表明，LncRNA OIP5-AS1通过调节miR-410-3p / Wnt7b信号通路促进了Wnt / β-肌动蛋白信号通路的激活，从而参与了RA的发生和发展。

LncRNA OIP5-AS1 has a common gene imbalance in various cancers and tumours, which plays an important role in regulating its biological function. However, there are few studies on lncRNA OIP5-AS1 in rheumatoid arthritis (RA). The purpose of the present study was to investigate the role of lncRNA OIP5-AS1 in the pathogenesis of RA. In the present study, we established an adjuvant arthritis (AA) rat model to obtain primary fibroblast-like synoviocytes (FLSs);The subcellular localisation of lncRNA OIP5-AS1 was detected by fluorescence in situ hybridisation (FISH) assay; Cell proliferation of FLSs was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay;IL-1β, IL-6 and TNF-α concentrations were measured by enzyme-linked immunosorbent assay (ELISA);Quantitative real-time PCR (qRT-PCR), Western blots(WB) and immunofluorescence were used to detect the expression of lncRNA OIP5-AS1/miR-410-3p/wnt7b signal axis and Wnt/β-catenin signal pathway related indicators in FLSs. FISH assay confirmed the presence of lncRNA OIP5-AS1 in the cytoplasm, suggesting that it acts as a competing endogenous RNA (ceRNA). qRT-PCR showed that the expression of lncRNA OIP5-AS1 was upregulated in FLSs, while the expression of miR-410-3p was downregulated in FLSs. We also found that lncRNA OIP5-AS1 knockdown inhibited the proliferation and inflammation of FLSs. Moreover, the expression of Wnt7b, the downstream target gene of miR-410-3p, and the activation of the Wnt/β-catenin signalling pathway were also inhibited by lncRNA OIP5-AS1 knockdown. These results suggested that lncRNA OIP5-AS1 promotes the activation of the Wnt/β-catenin signalling pathway by regulating the miR-410-3p/Wnt7b signalling axis, thereby participating in the occurrence and development of RA.