Abstract
Introduction: Growing evidence suggests that long non-coding RNA (lncRNA) GAS5 plays a critical role in inflammatory responses such as arthritis. In this study, we explored the function of GAS5 in acute gouty arthritis (AGA) and elucidated how GAS5 acts. Material and methods: RT-qPCR was used to examine GAS5 expression levels in serum. Receiver operating characteristic (ROC) curve analysis was used to explore the diagnostic value of GAS5. The THP-1 cell model of AGA was established by monosodium urate (MSU) in vitro. The pro-inflammation cytokines interleukin (IL)-1 β, IL-8, and tumor necrosis factor α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). Bioinformatics analysis, correlation analysis, and dual luciferase reporter assay were performed for the target association between miR-485-5p and GAS5. Results: GAS5 was suppressed in AGA patients, accompanied by upregulation of miR-485-5p. A high correlation between GAS5 and miR-485-5p was found, and GAS5 was associated with clinical characteristics in varying degrees. GAS5 achieved excellent performance accuracy, with the area under the ROC (AUC) of 0.915. Additionally, MSU-induced inflammatory responses were relieved through the overexpression of GAS5 in the cell model, while miR-485-5p overexpression reversed the responsiveness. The link between miR-485-5p and GAS5 was established in MSU-induced THP-1 macrophages. Conclusions: In summary, GAS5 alleviated MSU-induced excessive inflammation in THP-1 macro- phages by targeting miR-485-5p, suggesting that GAS5 is a potential diagnostic biomarker for AGA treatment.