ArticlePloS one2023
Therapeutic effect and mechanism of Daikenchuto in a model of methotrexate-induced acute small intestinal mucositis.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Curcumin treatment attenuates methotrexate-induced nephrotoxicity in rats by inhibiting inflammation and fibrosis.Journal of molecular histology · 2026Article
- Association Between Complementary Use of Daikenchuto (a Japanese Herbal Medicine) and Readmission in Older Patients With Heart Failure and Constipation.Circulation reports · 2025Article
- Mitigation of Methotrexate-Induced Intestinal Mucositis in Male Wistar Rats by Gallic Acid: The Role of HGF and C-Met Genes.Journal of toxicology · 2025Article
- Daikenchuto improves methotrexate-induced chronic small intestinal mucositis by promoting angiogenesis.Frontiers in pharmacology · 2025Article
- Molecular mechanisms underlying methotrexate-induced intestinal injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Use of Traditional Japanese Herbal Medicine Daikenchuto for the Treatment of Abdominal Distention in Very-Low-Birth-Weight Infants.Journal of clinical medicine · 2024Article
- Daikenchuto, a Japanese herbal medicine, ameliorates experimental colitis in a murine model by inducing secretory leukocyte protease inhibitor and modulating the gut microbiota.Frontiers in immunology · 2024Article
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDaikenchuto (DKT) has positive therapeutic effects on improving various gastrointestinal disorders. The present study investigated whether or not DKT has a potential therapeutic effect on chemotherapy-induced acute small intestinal mucositis (CIM) in a rat model.
methodsIntraperitoneal injection of 10 mg/kg methotrexate (MTX) every 3 days for a total of 3 doses was used for induction of CIM in a rat model. The MTX and DKT-MTX groups were injected with MTX as above from the first day, and the DKT-MTX and DKT groups were administered 2.7% DKT via the diet at the same time. The rats were euthanized on day 15.
resultsThe DKT-MTX group showed an improvement in the body weight and conditions of gastrointestinal disorders as well as increased levels of diamine oxidase in plasma and in the small intestinal villi. The pathology results showed that small intestinal mucosal injury in the DKT-MTX group was less severe than that in the MTX group. Immunohistochemistry for myeloperoxidase and malondialdehyde and quantitative real-time polymerase chain reaction (RT-qPCR) for TGF-β1 and HIF-1α showed that DKT attenuated peroxidative damage. The crypts in the DKT-MTX group contained more Ki-67-positive cells than MTX group. The zonula occluden-1 and claudin-3 results showed that DKT promoted repair of the mucosal barrier. RT-qPCR for the amino acid transporters EAAT3 and BO+AT also confirmed that DKT promoted mucosal repair and thus promoted nutrient absorption.
conclusionDKT protected against MTX-induced CIM in a rat model by reducing inflammation, stimulating cell proliferation, and stabilizing the mucosal barrier.
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