The Traditional Chinese Medicine Compound Huangqin Qingre Chubi Capsule Inhibits the Pathogenesis of Rheumatoid Arthritis Through the CUL4B/Wnt Pathway

被引:34
作者
Wang, Xiao [1 ]
Chang, Jun [2 ]
Zhou, Guoliang [3 ]
Cheng, Chenglong [4 ]
Xiong, Youyi [3 ]
Dou, Jinfeng [3 ]
Cheng, Gen [3 ]
Miao, Chenggui [4 ]
机构
[1] Anhui Univ Chinese Med, Sch Nursing, Dept Clin Nursing, Hefei, Peoples R China
[2] Anhui Med Univ, Affiliated Hosp 4, Dept Orthopaed, Hefei, Peoples R China
[3] Anhui Univ Sci & Technol, Sch Life & Hlth Sci, Dept Pharm, Fengyang, Peoples R China
[4] Anhui Univ Chinese Med, Sch Integrated Chinese & Western Med, Dept Pharmacol, Hefei, Peoples R China
基金
美国国家科学基金会;
关键词
rheumatoid arthritis; cullin; 4B; circ_0015756; canonical wnt signaling; huangqin qingre chubi capsule; CANONICAL WNT PATHWAY; SIGNALING PATHWAY; RATS;
D O I
10.3389/fphar.2021.750233
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The pathogenesis of rheumatoid arthritis (RA) is still not fully clarified, and the development of therapeutic drugs for RA is particularly urgent. Our group studies a possibility that circ_0015756/miR-942-5p may participate in the pathogenesis of RA through disordered Cullin 4B (CUL4B) and the traditional Chinese medicine compound Huangqin Qingre Chubi Capsule (HQC) may inhibit the pathogenesis of RA through the CUL4B/Wnt pathway. Data showed that the expression of circ_0015756 increased not only in fibroblast-like synoviocytes (FLS) of RA, but also in synovium and FLS of CIA mice, and the expression of miR-942-5p decreased. Abnormal circ_0015756 up-regulated the CUL4B expression and activated the canonical Wnt signaling pathway by inhibiting the expression of miR-942-5p. Circ_0015756 participated in the pathogenesis of RA and promoted the abnormal proliferation of FLS. Further, circ_0015756 activated the secretion of IL-1 and IL-8 and promoted the production of RA pathological gene MMP3 and fibronectin. Further analysis showed that HQC inhibited the pathogenesis of RA through the CUL4B/Wnt pathway, and the specific target was CUL4B. HQC interfered with the effects of circ_0015756 on the pathogenesis of RA by inhibiting the CUL4B, showing a good therapeutic effect on RA.
引用
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页数:14
相关论文
共 37 条
[1]   Wnt Signaling and Biological Therapy in Rheumatoid Arthritis and Spondyloarthritis [J].
Cici, Daniela ;
Corrado, Addolorata ;
Rotondo, Cinzia ;
Cantatore, Francesco P. .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2019, 20 (22)
[2]   Fibroblast-Like Synoviocytes Glucose Metabolism as a Therapeutic Target in Rheumatoid Arthritis [J].
de Oliveira, Patricia Gnieslaw ;
Farinon, Mirian ;
Sanchez-Lopez, Elsa ;
Miyamoto, Shigeki ;
Guma, Monica .
FRONTIERS IN IMMUNOLOGY, 2019, 10 :1743
[3]   Rheumatoid Arthritis Pathogenesis, Prediction, and Prevention: An Emerging Paradigm Shift [J].
Deane, Kevin D. ;
Holers, V. Michael .
ARTHRITIS & RHEUMATOLOGY, 2021, 73 (02) :181-193
[4]   Methotrexate mechanism in treatment of rheumatoid arthritis [J].
Friedman, Benjamin ;
Cronstein, Bruce .
JOINT BONE SPINE, 2019, 86 (03) :301-307
[5]  
Guo Jin-Chen, 2020, Zhongguo Zhong Yao Za Zhi, V45, P3228, DOI 10.19540/j.cnki.cjcmm.20200427.502
[6]   Epigenetic Regulation Mediated by Methylation in the Pathogenesis and Precision Medicine of Rheumatoid Arthritis [J].
Guo, Shicheng ;
Xu, Lingxia ;
Chang, Cen ;
Zhang, Runrun ;
Jin, Yehua ;
He, Dongyi .
FRONTIERS IN GENETICS, 2020, 11
[7]  
Huang Dan, 2020, Zhongguo Zhong Yao Za Zhi, V45, P451, DOI 10.19540/j.cnki.cjcmm.20190619.501
[8]   Activating Wnt/β-catenin signaling pathway for disease therapy: Challenges and opportunities [J].
Huang, Piao ;
Yan, Rong ;
Zhang, Xue ;
Wang, Lei ;
Ke, Xisong ;
Qu, Yi .
PHARMACOLOGY & THERAPEUTICS, 2019, 196 :79-90
[9]   The Role of WNT in Rheumatoid Arthritis and its Therapeutic Implication [J].
Imai, Kazushi ;
Chiba, Tadashige ;
Maeda, Genta ;
Morikawa, Masako .
MINI-REVIEWS IN MEDICINAL CHEMISTRY, 2009, 9 (03) :318-323
[10]   Abnormal level of CUL4B-mediated histone H2A ubiquitination causes disruptive HOX gene expression [J].
Lin, Ye ;
Yu, Juan ;
Wu, Jianxin ;
Wang, Shan ;
Zhang, Ting .
EPIGENETICS & CHROMATIN, 2019, 12 (1)