ArticleWorld journal of gastroenterology2023
Curcumin alleviated dextran sulfate sodium-induced colitis by recovering memory Th/Tfh subset balance.
Article in World journal of gastroenterology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.Signal transduction and targeted therapy · 2026Review
- Echinacea Purpurea Polysaccharides Alleviate DSS-Induced Colitis in Rats by Regulating Gut Microbiota and Short-Chain Fatty Acid Metabolism.Foods (Basel, Switzerland) · 2026Article
- The Construction Strategy of Curcumin Nanomedicine Delivery System and Its Application in the Treatment of Ulcerative Colitis.International journal of nanomedicine · 2025Review
- Ulcerative colitis: molecular insights and intervention therapy.Molecular biomedicine · 2024Review
- Use of curcumin and its nanopreparations in the treatment of inflammatory bowel disease.World journal of gastroenterology · 2024Article
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Authors and funding
10 authors.
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Abstract
backgroundRestoration of immune homeostasis by targeting the balance between memory T helper (mTh) cells and memory follicular T helper (mTfh) cells is a potential therapeutic strategy against ulcerative colitis (UC). Because of its anti-inflammatory and immunomodulatory properties, curcumin (Cur) is a promising drug for UC treatment. However, fewer studies have demonstrated whether Cur can modulate the mTh/mTfh subset balance in mice with colitis.
aimTo explore the potential mechanism underlying Cur-mediated alleviation of colitis induced by dextran sulfate sodium (DSS) in mice by regulating the mTh and mTfh immune homeostasis.
methodsBalb/c mice were administered 3% and 2% DSS to establish the UC model and treated with Cur (200 mg/kg/d) by gavage on days 11-17. On the 18
resultsCur effectively mitigates DSS-induced colitis, facilitates the restoration of mouse weight and colonic length, and diminishes the colonic weight and colonic weight index. Simultaneously, it hinders ulcer development and inflammatory cell infiltration in the colonic mucous membrane. While the percentage of Th1, mTh1, Th7, mTh7, Th17, mTh17, Tfh1, mTfh1, Tfh7, mTfh7, Tfh17, and mTfh17 cells decreased after Cur treatment of the mice for 7 d, and the frequency of mTh10, Th10, mTfh10, and Tfh10 cells in the mouse spleen increased. Further studies revealed that Cur administration prominently decreased the SOCS-1, SOCS-3, STAT3, p-STAT3, JAK1, p-JAK1, and NF-κB p65 protein expression levels in the colon tissue.
conclusionCur regulated the mTh/mTfh cell homeostasis to reduce DSS-induced colonic pathological damage, potentially by suppressing the JAK1/STAT3/SOCS signaling pathway.
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