The Huayu-Qiangshen-Tongbi (HQT) decoction, a Chinese medical formula, has been identified to show a potent therapeutic effect on rheumatoid arthritis (RA). However, the specific molecular mechanism of HQT in RA has not been well studied. In the present study, LPS-treated human rheumatoid fibroblast-like synoviocyte (FLS) MH7A cells and collagen-induced arthritis (CIA) mice were utilized as and models. Our results demonstrated that HQT could efficiently inhibit RA-induced inflammation by reducing the production of cytokines including tumor necrosis factor alpha (TNF-), interleukin-1 beta (IL-1), and interleukin-6 (IL-6). Moreover, HQT significantly upregulated the expression of miR-125b. Besides, analysis of bioinformatics suggested casein kinase 2 (CK2) was a potential target of miR-125b. Luciferase reporter assay was performed and revealed that miR-125b suppressed CK2 expression in MH7A cells. Furthermore, miR-125b inhibited LPS-induced NF-kappa-B (NF-B) activation, which is a downstream target of CK2. In addition, the NF-B inhibitor ammonium pyrrolidinedithiocarbamate (PDTC) and NF-kappa-B inhibitor alpha (IkB-) enhanced the inhibitory effect of miR-125b on the expression of TNF-, IL-1, and IL-6. Taken together, our study revealed that HQT could attenuate RA through upregulating miR-125b to suppress NF-B-induced inflammation by targeting CK2. The findings of this study should facilitate investigating the mechanism of HQT on RA and discovering novel therapeutic targets for RA.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9273410PMC
http://dx.doi.org/10.1155/2022/2836128DOI Listing

Publication Analysis

Top Keywords

rheumatoid arthritis
8
upregulating mir-125b
8
mir-125b suppress
8
suppress nf-b-induced
8
nf-b-induced inflammation
8
inflammation targeting
8
targeting ck2
8
mechanism hqt
8
mh7a cells
8
mir-125b
7

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!