LncRNA SNHG3 discriminates rheumatoid arthritis from healthy individuals and regulates inflammatory response and oxidative stress via modulating miR-128-3p.

Abstract

This study evaluated the expression and significance of SNHG3 in rheumatoid arthritis (RA), aiming to explore a biomarker and regulator for RA. The expression of SNHG3 in serum and synovial tissue was compared between RA patients and healthy individuals using polymerase chain reaction (PCR). The RA animal models were induced by the Porcine Type II collagen in Wistar rats and validated by the foot volume and arthritis index score. The human fibroblast-like synoviocytes were treated with lipopolysaccharide (LPS) to mimic the injury during RA onset, and the cell growth was assessed by cell counting kit-8 (CCK8) assay. SNHG3 was significantly downregulated in the serum and synovial tissue of RA patients compared with healthy individuals. Downregulated SNHG3 could discriminate RA patients from healthy individuals with high sensitivity (0.875) and specificity (0.844). Porcine Type II collagen induced increasing foot volume and arthritis index scores of rats, and SNHG3 was downregulated in RA rats. In LPS-induced human fibroblast-like synoviocytes, SNHG3 negatively regulated miR-128-3p, and the alleviated effect of SNHG3 overexpression on cellular inflammation and oxidative stress was reversed by miR-128-3p upregulation. Serum SNHG3 was considered a potential diagnostic biomarker for RA from healthy individuals. SNHG3 regulated inflammatory response and oxidative stress by negatively modulating miR-128-3p.