ArticleFrontiers in immunology2026
Catalpol mitigates rheumatoid arthritis by targeting neutrophil extracellular trap release.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Neutrophils: The Overlooked Regenerative Role in Bone Repair.Stem cell reviews and reports · 2026Review
- Systemic regulation of rheumatoid arthritis by mesenchymal stem cells: from immune homeostasis to microbiota modulation.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent synovial inflammation, progressive joint damage, and systemic manifestations. Current therapies, including NSAIDs, DMARDs, and biologics, face limitations such as side effects and high costs. Neutrophil extracellular traps (NETs), driven by peptidylarginine deiminase 4 (PAD4), play a pivotal role in RA pathogenesis by promoting inflammation and cartilage degradation. Catalpol (CAT), an iridoid glycoside known for its anti-inflammatory properties, exhibits therapeutic promise through targeting NET-related mechanisms. Methods: A collagen-induced arthritis (CIA) model was established in male DBA/1 mice. Mice were treated with CAT (30 mg/kg) or vehicle. Joint damage was assessed via micro-CT and histological staining (H&E, Safranin O, Toluidine Blue). NETs and inflammatory markers were analyzed by immunohistochemistry, Western blot, qRT-PCR, and immunofluorescence. Isolated neutrophils were stimulated with PMA Results: CAT treatment significantly ameliorated ankle swelling, bone erosion, synovial hyperplasia, inflammatory cell infiltration, and cartilage degradation in CIA mice. It suppressed the expression of NET-associated markers (Cit-H3, MPO, NE) and pro-inflammatory cytokines (IL-1β, IL-6) in joint tissues. CAT also inhibited the expression of matrix-degrading enzymes (MMP3, MMP13) and osteoclast-related factors (MMP9, CTSK, Tracp-5b). Conclusion: Catalpol exerts a protective effect in the CIA model by inhibiting PAD4-mediated NET formation, thereby reducing synovial inflammation, cartilage degradation, and bone erosion. Our findings highlight NETs as a promising therapeutic target and suggest catalpol's potential as a novel agent for RA treatment.
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Registered trials
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