Gout is caused by the accumulation of deposited monosodium urate (MSU) crystals in the joints. Recent studies have shown that interleukin-1β (IL-1β) is a key inflammatory mediator of acute gouty arthritis (AGA), and its level is regulated by microRNAs (miRNAs). The purpose of this study was to study the role of miR-221-5p in the pathogenesis of AGA.
One hundred patients with AGA and 94 healthy individuals were recruited. The expression of serum miR-221-5p was determined by quantitative real-time polymerase chain reaction. The receiver operating curve (ROC) was applied for diagnostic value analysis. A luciferase reporter assay was performed to confirm the interaction of miRNA and the 3'-untranslated region (UTR) of IL-1β. Enzyme-linked immunosorbent assay was used to detect serum and proinflammatory factors.
miR-221-5p had lower expression in the serum of AGA patients. The area under the curve was 0.884, the sensitivity was 82.0%, and the specificity was 80.9%. Serum miR-221-5p was negatively correlated with the expression levels of visual analog scale and IL-1β. Cell experiments showed that overexpression of miR-221-5p significantly inhibited the expression of inflammatory factors tumor necrosis factor-α, IL-8, and IL-1β, while down-regulation of miR-221-5p was the opposite. Luciferase analysis showed that IL-1β was the target gene of miR-221-5p.
This study confirmed that miR-221-5p regulates the production of inflammatory cytokines during the pathogenesis of AGA. These results suggested that miR-221-5p could be used as a potential therapeutic target for the treatment of AGA.