MiRNA-23a-5p is the biomarkers for gouty arthritis and promotes inflammation in rats of gouty arthritis via MyD88/NF-κB pathway by induction TLR2

被引:9
作者
Li, Fang [1 ]
Yao, Jian-Hua [2 ]
Li, Li [3 ]
Nie, Qian [4 ]
Cao, Jing-Jing [1 ]
Ning, Xiao-Ran [1 ]
机构
[1] Hebei Gen Hosp, Dept Rheumatism & Immunol, Shijiazhuang, Hebei, Peoples R China
[2] Hebei Med Univ, Dept Geratol, Hosp 2, Shijiazhuang, Hebei, Peoples R China
[3] Hebei Gen Hosp, Dept Ultrasonograph, Shijiazhuang, Hebei, Peoples R China
[4] Hebei Gen Hosp, Medicai Examinat Ctr, Shijiazhuang, Hebei, Peoples R China
关键词
Gouty arthritis; inflammation; miRNA-23a-5p; MyD88; NF; kappa B; TLR2; FIBROBLAST-LIKE SYNOVIOCYTES; NF-KAPPA-B; EXPRESSION; MYD88;
D O I
10.46497/ArchRheumatol.2022.9236
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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-kB) 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-kappa B pathway by targeting TLR2.
引用
收藏
页码:536 / 546
页数:11
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