ArticleBritish journal of pharmacology2018
Cambogin suppresses dextran sulphate sodium-induced colitis by enhancing Treg cell stability and function.
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Oxymatrine for inflammatory bowel disease in preclinical studies: a systematic review and meta-analysis.Frontiers in medicine · 2025Pooled it
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- Chronic DSS-Induced Colitis Exacerbates Parkinson's Disease Phenotype and Its Pathological Features Following Intragastric Rotenone Exposure.ACS pharmacology & translational science · 2025Article
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- Ubiquitin-Specific Peptidase 7: A Novel Deubiquitinase That Regulates Protein Homeostasis and Cancers.Frontiers in oncology · 2021Review
- Berberis lycium fruit extract attenuates oxi-inflammatory stress and promotes mucosal healing by mitigating NF-κB/c-Jun/MAPKs signalling and augmenting splenic Treg proliferation in a murine model of dextran sulphate sodium-induced ulcerative colitis.European journal of nutrition · 2020Article
- YYFZBJS ameliorates colorectal cancer progression in ApcCell communication and signaling : CCS · 2020Article
- The Active Ingredients Identification and Antidiarrheal Mechanism Analysis ofFrontiers in pharmacology · 2020Article
- Tryptophan Metabolism, Regulatory T Cells, and Inflammatory Bowel Disease: A Mini Review.Mediators of inflammation · 2020Review
- Protective effects of oxymatrine against DSS-induced acute intestinal inflammation in mice via blocking the RhoA/ROCK signaling pathway.Bioscience reports · 2019Article
- Purification of 3, 4-dihydroxyphenylethyl alcohol glycoside from Sargentodoxa cuneata (Oliv.) Rehd. et Wils. and its protective effects against DSS-induced colitis.Scientific reports · 2019Article
- Gaudichaudione H Inhibits Inflammatory Responses in Macrophages and Dextran Sodium Sulfate-Induced Colitis in Mice.Frontiers in pharmacology · 2019Article
- Cambogin suppresses dextran sulphate sodium-induced colitis by enhancing Treg cell stability and function.British journal of pharmacology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeInflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gastrointestinal tract, and an impaired immune response plays a critical role in IBD. The current drugs and therapies for IBD treatment are of limited use, therefore, there is a need to find novel drugs or therapies for this disease. We investigated the effect of cambogin in a mouse model of dextran sulphate sodium (DSS)-induced colitis and whether cambogin attenuates inflammation via a Treg-cell-mediated effect on the immune response. EXPERIMENTAL APPROACH: Chronic colitis was established in mice using 2% DSS, and cambogin (10 mg·kg KEY
resultsCambogin attenuated diarrhoea, colon shortening and colon histological injury and IL-6, IFN-γ and TNF-α production in DSS-treated mice. Cambogin also up-regulated Treg cell numbers in both the spleen and mesenteric lymph nodes. Furthermore, cambogin (10 μM) prevented Foxp3 loss in human primary Treg cells in vitro, and promoted USP7-mediated Foxp3 deubiquitination and increased Foxp3 protein expression in LPS-treated cells. CONCLUSIONS AND IMPLICATIONS: The effect of cambogin on DSS-induced colitis is expedited by a Treg-cell-mediated modification of the immune response, suggesting that cambogin could be applied as a novel agent for treating colitis and other Treg cell-related diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.