صورة الغلاف

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

محفوظ في:
الحاوية / القاعدة:International Journal of Immunopathology and Pharmacology vol. 39 (Jun 2025)
المؤلف الرئيسي: Shu-Ping, Kung
مؤلفون آخرون: Hira, Umbreen, Wang Jou-Hsuan, Chih-Ming, Tsia, Lin Tim Chi-Chen, Yu-Ting, Chen
منشور في:
Sage Publications Ltd.
الموضوعات:
Central Intelligence Agency > CIA
Helper cells
Molecular modelling
Rheumatoid arthritis
Cell differentiation
Phosphorylation
Tumor necrosis factor-α
Autoimmune diseases
Lymphocytes T
Collagen
Stat3 protein
Inflammation
الوصول للمادة أونلاين:Citation/Abstract
الوسوم: إضافة وسم
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مستخلص: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.
تدمد:0394-6320
2058-7384
DOI:10.1177/03946320251348715
المصدر:Health & Medical Collection