Fang Li1, Jian-Hua Yao2, Li Li3, Qian Nie4, , Jing-Jing Cao1, Xiao-Ran Ning1

1Department of Rheumatism and Immunology, Hebei General Hospital, Shijiazhuang, China
2Department of Geratology, The Second Hospital of Hebei Medical University, Shijiazhuang, China
3Department Ultrasonograph, Hebei General Hospital, Shijiazhuang, China
4Hebei General Hospital, Medicai Examination Center, Shijiazhuang, China

Keywords: Gouty arthritis, inflammation, miRNA-23a-5p, MyD88, NF-κB, TLR2.


Objectives: In this study, we aimed to examine the efficacy of micro ribonucleic acid (miRNA)-23a-5p in gouty arthritis and to investigate its possible mechanism.

Materials and methods: Gouty arthritis in rat was established by intraarticular injection of 0.2 mL monosodium urate crystal (20 mg/mL) inside knee joint cavity. THP-1 cell was induced using lipopolysaccharides (LPS) for in vitro model.

Results: Serum miRNA-23a-5p expression levels were increased in rats of gouty arthritis. However, overexpression of miRNA-23a-5p promoted inflammation and induced myeloid differential protein-88 (MyD88)/nuclear factor-kappa B (NF-κB) pathway by induction toll-like receptor-2 (TLR2) in vitro. The inhibition of TLR2 attenuated the pro-inflammation effects of miRNA-23a-5p in inflammation in in vitro model of gouty arthritis.

Conclusion: Our findings demonstrate that miRNA-23a-5p is a biomarker for gouty arthritis and promotes inflammation in rats of gouty arthritis via MyD88/NF-κB pathway by targeting TLR2.