ArticleBlood cells, molecules & diseases2016
Dietary supplementation with ipriflavone decreases hepatic iron stores in wild type mice.
Article in Blood cells, molecules & diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Iron Deficiency and Iron Deficiency Anemia: A Comprehensive Overview of Established and Emerging Concepts.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Metabolic dysregulation in myelodysplastic neoplasm: impact on pathogenesis and potential therapeutic targets.Medical oncology (Northwood, London, England) · 2024Review
- Intraamniotic Administration (Nutrients · 2022Article
- Pharmacological implications of ipriflavone against environmental metal-induced neurodegeneration and dementia in rats.Environmental science and pollution research international · 2021Article
- Therapeutic Advances in Regulating the Hepcidin/Ferroportin Axis.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Role of Dietary Flavonoids in Iron Homeostasis.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Quercetin inhibits intestinal non-haem iron absorption by regulating iron metabolism genes in the tissues.European journal of nutrition · 2019Article
- Hepcidin Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Nicotinamide N-methyltransferase expression decreases in iron overload, exacerbating toxicity in mouse hepatocytes.Hepatology communications · 2017Article
- Imatinib and spironolactone suppress hepcidin expression.Haematologica · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Hepcidin, a peptide produced in the liver, decreases intestinal iron absorption and macrophage iron release by causing degradation of the iron exporter, ferroportin. Because its levels are inappropriately low in patients with iron overload syndromes, hepcidin is a potential drug target. We previously conducted a chemical screen that revealed ipriflavone, an orally available small molecule, as a potent inducer of hepcidin expression. To evaluate ipriflavone's effect on iron homeostasis, we placed groups of 5-week old wild type or thalassemia intermedia (Hbb(Th3+/-)) mice on a soy-free, iron-sufficient diet, AIN-93G containing 220mg iron and 0-750mgipriflavone/kg of food for 50days. Ipriflavone 500mg/kg significantly reduced liver iron stores and intestinal ferroportin expression in WT mice, while increasing the ratio of hepcidin transcript levels to liver iron stores. Ipriflavone supplementation in Hbb(Th3+/-) mice failed to alleviate iron overload and was associated with a milder reduction in intestinal ferroportin and a failure to alter the ratio of hepcidin transcript levels to liver iron stores or splenic expression of the hepcidin-regulatory hormone, erythroferrone. These data suggest that dietary supplementation with ipriflavone alone would not be sufficient to treat iron overload in thalassemia intermedia.
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Registered trials
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