Cucurbitacin B inhibits Th17 cell differentiation via the suppression of the JAK/STAT pathway and alleviates collagen-induced arthritis in mice

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Publicat a:International Journal of Immunopathology and Pharmacology vol. 39 (Jun 2025)
Autor principal: Shu-Ping, Kung
Altres autors: Hira, Umbreen, Wang Jou-Hsuan, Chih-Ming, Tsia, Lin Tim Chi-Chen, Yu-Ting, Chen
Publicat:
Sage Publications Ltd.
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Accés en línia:Citation/Abstract
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LEADER 00000nab a2200000uu 4500
001 3287004908
003 UK-CbPIL
022 |a 0394-6320 
022 |a 2058-7384 
024 7 |a 10.1177/03946320251348715  |2 doi 
035 |a 3287004908 
045 2 |b d20250601  |b d20250630 
100 1 |a Shu-Ping, Kung  |u Department of Pathology and Laboratory Medicine, Taichung Veterans General Hospital, Taiwan, China, R.O.C. 
245 1 |a Cucurbitacin B inhibits Th17 cell differentiation via the suppression of the JAK/STAT pathway and alleviates collagen-induced arthritis in mice 
260 |b Sage Publications Ltd.  |c Jun 2025 
513 |a Journal Article 
520 3 |a Objective: Rheumatoid arthritis (RA) is a chronic autoimmune disease with limited treatment options and associated side effects or resistance. This study aims to investigate the therapeutic potential of the natural compound cucurbitacin B (CuB) in RA treatment. Methods: We utilized a collagen-induced arthritis (CIA) mouse model to evaluate the effects of CuB. Arthritis scores, histological damage, and pro-inflammatory cytokine expression (TNF-α, IL-17A) were assessed. In addition, network pharmacology analysis was performed to explore CuB’s molecular mechanisms, focusing on Th17 cell differentiation, IL-17 signaling, and the JAK-STAT pathway. Results: CuB significantly reduced arthritis severity, decreased histological damage, and lowered the expression of pro-inflammatory cytokines in CIA mice. CuB was found to inhibit STAT3 phosphorylation and reduce the proportion of Th17 cells in the spleen, indicating its potential anti-inflammatory effects. Conclusion: These findings suggest that cucurbitacin B may serve as a promising novel therapeutic agent for rheumatoid arthritis by targeting key inflammatory pathways. 
610 4 |a Central Intelligence Agency--CIA 
653 |a Helper cells 
653 |a Molecular modelling 
653 |a Rheumatoid arthritis 
653 |a Cell differentiation 
653 |a Phosphorylation 
653 |a Tumor necrosis factor-α 
653 |a Autoimmune diseases 
653 |a Lymphocytes T 
653 |a Collagen 
653 |a Stat3 protein 
653 |a Inflammation 
700 1 |a Hira, Umbreen  |u Institute of Biomedical Science, National Chung Hsing University, Taichung, Taiwan, China, R.O.C. 
700 1 |a Wang Jou-Hsuan  |u Department of Physical Medicine and Rehabilitation, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan, China, R.O.C. 
700 1 |a Chih-Ming, Tsia  |u Division of Infectious Diseases, Department of Pediatrics, University of California, La Jolla, CA, USA, R.O.C. 
700 1 |a Lin Tim Chi-Chen  |u Department of Pathology and Laboratory Medicine, Taichung Veterans General Hospital, Taiwan, China, R.O.C. 
700 1 |a Yu-Ting, Chen  |u Graduate Institute of Genomics and Bioinformatics, National Chung Hsing University, Taichung, Taiwan, China, R.O.C. 
773 0 |t International Journal of Immunopathology and Pharmacology  |g vol. 39 (Jun 2025) 
786 0 |d ProQuest  |t Health & Medical Collection 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3287004908/abstract/embedded/L8HZQI7Z43R0LA5T?source=fedsrch