ArticleFrontiers in pharmacology2016
Curcumin Suppressed Activation of Dendritic Cells via JAK/STAT/SOCS Signal in Mice with Experimental Colitis.
Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 96 citations in OpenAlex.
- Curcumin (The Journal of clinical and aesthetic dermatology · 2026Review
- Hepatoprotective Potential of Curcumin in the Prevention of Liver Dysfunction in a Porcine Model.Nutrients · 2026Review
- Obesity-Related Oxidative Stress and Antioxidant Properties of Natural Compounds in the Enteric Nervous System: A Literature Overview.Antioxidants (Basel, Switzerland) · 2026Review
- The role of dietary factors in the prevention and management of inflammatory bowel disease: a comprehensive review.Nutrition & metabolism · 2025Review
- The Significance of STAT3 in Colonic Diseases: A Comprehensive Study of Pathological Roles and Therapeutic Implications.Cell biochemistry and biophysics · 2025Review
- Curcumin for inflammatory bowel disease therapy: advances in mechanisms, clinical applications, and drug delivery.Archives of pharmacal research · 2025Review
- Quercetin pretreated umbilical cord mesenchymal stem cells alleviate inflammatory bowel diseaseWorld journal of stem cells · 2025Article
- Curcumin in Inflammatory Complications: Therapeutic Applications and Clinical Evidence.International journal of molecular sciences · 2025Review
- Carotenoids and Their Interaction with the Immune System.Antioxidants (Basel, Switzerland) · 2025Review
- Targeting JAK/STAT signaling pathway by curcumin: implications for spinal cord injury neuroprotection.Inflammopharmacology · 2025Review
- Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025Review
- Natural products for the treatment of ulcerative colitis: focus on the JAK/STAT pathway.Frontiers in immunology · 2025Review
- Phytochemicals as modulators of dendritic cell functions: implications for tolerogenic cell-based therapy.Frontiers in immunology · 2025Review
- Regulation mechanism of curcumin mediated inflammatory pathway and its clinical application: a review.Frontiers in pharmacology · 2025Review
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
- Ulcerative colitis: molecular insights and intervention therapy.Molecular biomedicine · 2024Review
- Curcumin as a regulator of Th17 cells: Unveiling the mechanisms.Food chemistry. Molecular sciences · 2024Review
- Mechanistic insight of curcumin: a potential pharmacological candidate for epilepsy.Frontiers in pharmacology · 2024Review
- Challenges and Future Trends in Atopic Dermatitis.International journal of molecular sciences · 2023Review
- Curcumin Alleviates Aflatoxin BFoods (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic cells (DCs) play a pivotal role as initiators in the pathogenesis of inflammatory bowel disease and are regulated by the JAK/STAT/SOCS signaling pathway. As a potent anti-inflammatory compound, curcumin represents a viable treatment alternative or adjunctive therapy in the management of chronic inflammatory bowel disease (IBD). The mechanism of curcumin treated IBD on DCs is not completely understood. In the present study, we explored the mechanism of curcumin treated experimental colitis by observing activation of DCs via JAK/STAT/SOCS signaling pathway in colitis mice. Experimental colitis was induced by 2, 4, 6-trinitrobenzene sulfonic acid. After 7 days treatment with curcumin, its therapeutic effect was verified by decreased colonic weight, histological scores, and remitting pathological injury. Meanwhile, the levels of major histocompatibility complex class II and DC costimulatory molecules (CD83, CD28, B7-DC, CD40, CD40 L, and TLR2) were inhibited and followed the up-regulated levels of IL-4, IL-10, and IFN-γ, and down-regulated GM-CSF, IL-12p70, IL-15, IL-23, and TGF-β1. A key finding was that the phosphorylation of the three members (JAK2, STAT3, and STAT6) of the JAK/STAT/SOCS signaling pathway was inhibited, and the three downstream proteins (SOCS1, SOCS3, and PIAS3) from this pathway were highly expressed. In conclusion, curcumin suppressed the activation of DCs by modulating the JAK/STAT/SOCS signaling pathway to restore immunologic balance to effectively treat experimental colitis.
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