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微小RNA-23a-5p是痛风性关节炎的生物标志物，通过诱导Toll样受体2（TLR2），经髓样分化因子88（MyD88）/核因子κB（NF-κB）信号通路促进痛风性关节炎大鼠的炎症反应。

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.

作者信息

Li Fang, Yao Jian-Hua, Li Li, Nie Qian, Cao Jing-Jing, Ning Xiao-Ran

机构信息

Department of Rheumatism and Immunology, Hebei General Hospital, Shijiazhuang, China.

Department of Geratology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

出版信息

Arch Rheumatol. 2022 Jul 29;37(4):536-546. doi: 10.46497/ArchRheumatol.2022.9236. eCollection 2022 Dec.

DOI:10.46497/ArchRheumatol.2022.9236
PMID:36879567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9985376/
Abstract

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 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) . The inhibition of TLR2 attenuated the pro-inflammation effects of miRNA-23a-5p in inflammation in 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.

摘要

目的

在本研究中，我们旨在检测微小核糖核酸（miRNA）-23a-5p在痛风性关节炎中的作用，并探究其可能的机制。

材料与方法

通过在大鼠膝关节腔内注射0.2 mL尿酸钠晶体（20 mg/mL）建立痛风性关节炎大鼠模型。使用脂多糖（LPS）诱导THP-1细胞作为模型。

结果

痛风性关节炎大鼠血清miRNA-23a-5p表达水平升高。然而，miRNA-23a-5p的过表达通过诱导Toll样受体2（TLR2）促进炎症反应并激活髓样分化蛋白88（MyD88）/核因子κB（NF-κB）信号通路。在痛风性关节炎模型中，抑制TLR2可减弱miRNA-23a-5p的促炎作用。

结论

我们的研究结果表明，miRNA-23a-5p是痛风性关节炎的生物标志物，并且通过靶向TLR2，经MyD88/NF-κB信号通路促进痛风性关节炎大鼠的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/de2b045f8351/AR-2022-37-4-536-546-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/19b1b0ac9e27/AR-2022-37-4-536-546-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/df37cec33a54/AR-2022-37-4-536-546-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/4c8080dff1d2/AR-2022-37-4-536-546-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/9448068173bd/AR-2022-37-4-536-546-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/f4f8d110ed1f/AR-2022-37-4-536-546-F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/de2b045f8351/AR-2022-37-4-536-546-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/19b1b0ac9e27/AR-2022-37-4-536-546-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/df37cec33a54/AR-2022-37-4-536-546-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/4c8080dff1d2/AR-2022-37-4-536-546-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/9448068173bd/AR-2022-37-4-536-546-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/f4f8d110ed1f/AR-2022-37-4-536-546-F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/9985376/de2b045f8351/AR-2022-37-4-536-546-F6.jpg

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