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氧化苦参碱通过调节 T 细胞免疫平衡缓解胶原诱导性关节炎小鼠的病情。

Oxymatrine Alleviates Collagen-Induced Arthritis in Mice by Regulating the Immune Balance of T Cells.

机构信息

Department of Pathogen Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.

出版信息

Molecules. 2023 Aug 4;28(15):5879. doi: 10.3390/molecules28155879.

DOI:10.3390/molecules28155879
PMID:37570855
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10420974/
Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by systemic immunity and autoimmune disorders. We have previously found that oxymatrine (OMT), a natural alkaloid, can alleviate rheumatoid arthritis without knowing whether OMT can alleviate rheumatoid arthritis through gut microbiota. In this study, we found that OMT can alleviate collagen-induced arthritis in mice and reconstruct the immune balance of Th1/Th2, Treg/Th17, and Tfr/Tfh cells. Colon transcriptome gene enrichment analysis indicated that oxymatrine may alleviate collagen induced arthritis in mice through immune system process pathway. Furthermore, OMT significantly altered the gut microbiota variety, changed the composition of microbial colonies, and reshaped the gut microbiota of collagen-induced arthritis (CIA) mice, which may participate in the regulation of the balance of Th1/Th2, Treg/Th17, and Tfr/Tfh cells to alleviate collagen-induced arthritis in mice.

摘要

类风湿关节炎(RA)是一种以全身免疫和自身免疫紊乱为特征的慢性自身免疫性疾病。我们之前发现苦参碱(OMT),一种天然生物碱,可以缓解类风湿关节炎,但不知道 OMT 是否可以通过肠道微生物群来缓解类风湿关节炎。在这项研究中,我们发现 OMT 可以缓解胶原诱导性关节炎(CIA)小鼠,并重建 Th1/Th2、Treg/Th17 和 Tfr/Tfh 细胞的免疫平衡。结肠转录组基因富集分析表明,苦参碱可能通过免疫系统过程途径缓解胶原诱导性关节炎的发生。此外,OMT 还显著改变了肠道微生物的多样性,改变了微生物群落的组成,并重塑了胶原诱导性关节炎(CIA)小鼠的肠道微生物群,这可能参与了调节 Th1/Th2、Treg/Th17 和 Tfr/Tfh 细胞的平衡,从而缓解 CIA 小鼠的关节炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/a496901eed14/molecules-28-05879-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/c375f7826c68/molecules-28-05879-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/b8d375b8e93f/molecules-28-05879-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/635b305afba4/molecules-28-05879-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/e4c6f8579ff9/molecules-28-05879-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/a496901eed14/molecules-28-05879-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/c375f7826c68/molecules-28-05879-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/b8d375b8e93f/molecules-28-05879-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/635b305afba4/molecules-28-05879-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/e4c6f8579ff9/molecules-28-05879-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e94/10420974/a496901eed14/molecules-28-05879-g005.jpg

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Efficacy of Janus kinase inhibitors in rheumatoid arthritis.
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Hsa_circ_0007707 participates in PDE3B-mediated apoptosis inhibition and inflammation promotion in fibroblast-like synoviocytes.Hsa_circ_0007707 参与成纤维样滑膜细胞中 PDE3B 介导的细胞凋亡抑制和炎症促进。
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