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

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

  • Int J Immunopathol Pharmacol. 2025 Jan-Dec:39:3946320251348715. doi: 10.1177/03946320251348715.
Shu-Ping Kung 1 2,  Hira Umbreen 2,  Jou-Hsuan Wang 3,  Chih-Ming Tsia 4,  Tim Chi-Chen Lin 1 5 6 7 8,  Yu-Ting Chen 9
Affiliations

Affiliations

  • 1 Department of Pathology and Laboratory Medicine, Taichung Veterans General Hospital, Taiwan, China, R.O.C.
  • 2 Institute of Biomedical Science, National Chung Hsing University, Taichung, Taiwan, China, R.O.C.
  • 3 Department of Physical Medicine and Rehabilitation, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan, China, R.O.C.
  • 4 Division of Infectious Diseases, Department of Pediatrics, University of California, La Jolla, CA, USA, R.O.C.
  • 5 Department of Medical Research, China Medical University Hospital, Taichung, Taiwan, China, R.O.C.
  • 6 Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan, China, R.O.C.
  • 7 Department of Pharmacology, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, China, R.O.C.
  • 8 The iEGG and Animal Biotechnology Center, National Chung Hsing University, Taichung, Taiwan, China, R.O.C.
  • 9 Graduate Institute of Genomics and Bioinformatics, National Chung Hsing University, Taichung, Taiwan, China, R.O.C.
PMID: 40518910 DOI: 10.1177/03946320251348715
Abstract

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.

Keywords

JAK/STAT pathway; Th17 cell differentiation; anti-inflammatory therapy; cucurbitacin B; rheumatoid arthritis (RA).

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