دورية أكاديمية

Quantitative proteomic analysis of circulating exosomes reveals the mechanism by which Triptolide protects against collagen‐induced arthritis.

التفاصيل البيبلوغرافية
العنوان: Quantitative proteomic analysis of circulating exosomes reveals the mechanism by which Triptolide protects against collagen‐induced arthritis.
المؤلفون: Liu, Xiuchan, Liu, Xu, Wang, Hui, Chen, Ming, Zhang, Geng, Ren, Dongyun, Zhang, Na, Wei, Wei
المصدر: Immunity, Inflammation & Disease; Jun2024, Vol. 12 Issue 6, p1-14, 14p
مصطلحات موضوعية: COLLAGEN-induced arthritis, EXOSOMES, TRIPTOLIDE, WESTERN immunoblotting, QUANTITATIVE research
مستخلص: Introduction: Triptolide (TP), a natural product derived from the herbal medicine Tripterygium wilfordii, exhibits potent immunosuppressive activity. However, the mechanisms underlying its effects in rheumatoid arthritis remain incompletely understood. Methods: Collagen‐induced arthritis (CIA) model was induced in Sprague−Dawley rats by immunization with bovine type II collagen, and TP was administrated as treatment. The therapeutic effect of TP was evaluated based on paw swelling, histopathology, and serum levels of inflammatory factors. Exosomes isolated from rat serum were characterized by transmission electron microscopy, dynamic light scattering, and western blot analysis. Proteomic profiling of exosomes was analyzed by direct DIA quantitative proteomics analysis. Gene ontology and the Kyoto Encyclopedia of Genes and Genomes databases were employed for enrichment analysis related to molecular function, biological processes, and signaling pathways. Western blot analysis was used to analyze differentially expressed proteins. Results: TP treatment ameliorated arthritic phenotypes in CIA rats as evidenced by reduced arthritis score, paw swelling, pathological injury severity scores, and serum levels of inflammatory cytokines. The proteomic analysis revealed that TP treatment significantly inhibited complement and coagulation cascades, interleukin‐17 signaling pathway, and cholesterol metabolism, which were reactivated in CIA rats. Importantly, lipocalin 2 (LCN2) and myeloperoxidase (MPO) levels were markedly upregulated in the CIA group but suppressed upon TP administration. Furthermore, in synovial tissues, LCN2 and MPO expression levels were also elevated in the CIA group but decreased following TP treatment. Conclusion: Our findings demonstrate that TP alleviates CIA, possibly through modulation of exosomal LCN2 and MPO proteins. [ABSTRACT FROM AUTHOR]
Copyright of Immunity, Inflammation & Disease is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
قاعدة البيانات: Complementary Index
الوصف
تدمد:20504527
DOI:10.1002/iid3.1322