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CS-semi5抑制核因子-κB激活，以阻断与胶原诱导性关节炎相关的滑膜炎症、软骨损伤和骨侵蚀。

CS-semi5 Inhibits NF-κB Activation to Block Synovial Inflammation, Cartilage Loss and Bone Erosion Associated With Collagen-Induced Arthritis.

作者信息

Li Xiang, Tang Xiaonan, Wang Yufei, Chai Changwei, Zhao Zhehui, Zhang Haijing, Peng Ying, Wu Lianqiu

机构信息

Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

出版信息

Front Pharmacol. 2021 Jul 9;12:655101. doi: 10.3389/fphar.2021.655101. eCollection 2021.

DOI:10.3389/fphar.2021.655101
PMID:34305585
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8298759/
Abstract

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease that affects 1% of the population. CS-semi5 is a semisynthetic chondroitin sulfate. In this study, CS-semi5 was shown to have positive effects on a model of collagen-induced arthritis (CIA). CS-semi5 treatment had obvious effects on weight loss and paw swelling in CIA mice. Post-treatment analysis revealed that CS-semi5 alleviated three main pathologies (i.e., synovial inflammation, cartilage erosion and bone loss) in a dose-dependent manner. Further study showed that CS-semi5 could effectively reduce TNF-α and IL-1β production in activated macrophages the NF-κB pathway. CS-semi5 also blocked RANKL-trigged osteoclast differentiation from macrophages. Therefore, CS-semi5 may effectively ameliorate synovial inflammation, cartilage erosion and bone loss in RA through NF-κB deactivation.

摘要

类风湿性关节炎（RA）是一种影响1%人口的慢性全身性自身免疫性疾病。CS-semi5是一种半合成硫酸软骨素。在本研究中，CS-semi5对胶原诱导性关节炎（CIA）模型显示出积极作用。CS-semi5治疗对CIA小鼠的体重减轻和爪肿胀有明显影响。治疗后分析显示，CS-semi5以剂量依赖的方式减轻了三种主要病理变化（即滑膜炎症、软骨侵蚀和骨质流失）。进一步研究表明，CS-semi5可有效降低活化巨噬细胞中TNF-α和IL-1β的产生以及NF-κB信号通路的活性。CS-semi5还阻断了RANKL触发的巨噬细胞向破骨细胞的分化。因此，CS-semi5可能通过使NF-κB失活而有效改善RA中的滑膜炎症、软骨侵蚀和骨质流失。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/81dc7fd7f81b/fphar-12-655101-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/a920666f73b8/fphar-12-655101-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/e22c9d242c94/fphar-12-655101-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/e0fe47623223/fphar-12-655101-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/af176fb57272/fphar-12-655101-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/32df6dce93b9/fphar-12-655101-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/2e0513198a8f/fphar-12-655101-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/73e0c5b9093d/fphar-12-655101-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/81dc7fd7f81b/fphar-12-655101-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/a920666f73b8/fphar-12-655101-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/e22c9d242c94/fphar-12-655101-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/e0fe47623223/fphar-12-655101-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/af176fb57272/fphar-12-655101-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/32df6dce93b9/fphar-12-655101-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/2e0513198a8f/fphar-12-655101-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/73e0c5b9093d/fphar-12-655101-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a06/8298759/81dc7fd7f81b/fphar-12-655101-g008.jpg

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引用本文的文献

[1]
Chondroitin Sulfate A-Selenium Nanoparticles Activate Autophagy Through the AMPK-mTOR Pathway to Alleviate Oxidative Stress and Mitochondrial Dysfunction to Repair Kashin-Beck Disease Chondrocytes.

Biol Trace Elem Res. 2025-7-15

[2]
Sex differences in long-term effects of collagen-induced arthritis in middle-aged mice.

Front Physiol. 2023-6-28

[3]
Chondroitin Sulfate Supplements for Osteoarthritis: A Critical Review.

Cureus. 2023-6-9

[4]
Combined treatment with glucosamine and chondroitin sulfate improves rheumatoid arthritis in rats by regulating the gut microbiota.

Nutr Metab (Lond). 2023-4-4

[5]
Myricitrin inhibits fibroblast-like synoviocyte-mediated rheumatoid synovial inflammation and joint destruction by targeting AIM2.

Front Pharmacol. 2022-8-31

[6]
Identification of Tissue-Specific Expressed Hub Genes and Potential Drugs in Rheumatoid Arthritis Using Bioinformatics Analysis.

Front Genet. 2022-3-18

本文引用的文献

[1]
Effects of Biological Therapies on Molecular Features of Rheumatoid Arthritis.

Int J Mol Sci. 2020-11-28

[2]
A biopolymer-based and inflammation-responsive nanodrug for rheumatoid arthritis treatment inhibiting JAK-STAT and JNK signalling pathways.

Nanoscale. 2020-11-26

[3]
Auranofin mitigates systemic iron overload and induces ferroptosis via distinct mechanisms.

Signal Transduct Target Ther. 2020-7-31

[4]
Macrophage M1/M2 polarization and rheumatoid arthritis: A systematic review.

Autoimmun Rev. 2019-9-11

[5]
The synthesis and biological evaluation of chondroitin sulfate E glycodendrimers.

Future Med Chem. 2019-7-15

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Chondroitin Sulfate Safety and Quality.

Molecules. 2019-4-12

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Nutrition, osteoarthritis and cartilage metabolism.

Aging Clin Exp Res. 2019-4-13

[8]
Flemingia philippinensis Flavonoids Relieve Bone Erosion and Inflammatory Mediators in CIA Mice by Downregulating NF-B and MAPK Pathways.

Mediators Inflamm. 2019-2-17

[9]
Melatonin attenuates TNF-α and IL-1β expression in synovial fibroblasts and diminishes cartilage degradation: Implications for the treatment of rheumatoid arthritis.

J Pineal Res. 2019-2-14

[10]
Is macrophage polarization important in rheumatoid arthritis?

Int Immunopharmacol. 2017-9

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