ArticleDigestive diseases and sciences2013
Glycyrrhizin enhances therapeutic activity of a colon-specific methylprednisolone prodrug against experimental colitis.
Article in Digestive diseases and sciences, 2013. 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, 8 citations in OpenAlex.
- Bioactive compounds of Glycyrrhiza glabra and their functional role in modulating gut inflammation and intestinal homeostasis.Inflammopharmacology · 2026Review
- Programmable saponin biosynthesis from gene networks to predictive biomanufacturing.Frontiers in plant science · 2026Review
- Glucocorticoids-based prodrug design: Current strategies and research progress.Asian journal of pharmaceutical sciences · 2024Review
- Terpenes: Modulating anti-inflammatory signaling in inflammatory bowel disease.Pharmacology & therapeutics · 2023Review
- Glycyrrhizic acid in the treatment of liver diseases: literature review.BioMed research international · 2014Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCo-administration of a reduction inhibitor and a colon-specific prodrug of a glucocorticoid susceptible to colonic reductive metabolism is suggested as a strategy to circumvent the therapeutic loss of the glucocorticoid delivered to and acting locally at the large intestine.
aimsWe examined whether the strategy was feasible as a pharmacotherapy for treatment of inflammatory bowel disease.
methodsGlycyrrhizin (GCZ), a reduction inhibitor, was tested for its inhibition of the colonic metabolism of methylprednisolone (MP). Therapeutic activity against TNBS-induced rat colitis and adrenal suppression were compared after oral administration of methylprednisolone 21-sulfate sodium (MPS), a colon-specific prodrug of MP, or MPS/GCZ to colitic rats.
resultsUpon incubation of MP with the cecal contents, MP disappeared, and this was delayed by addition of GCZ. In addition, more MP produced from MPS in the cecal contents accumulated in the presence of GCZ. Consistent with these results, upon oral administration of MPS/GCZ, MPS or MP, MP was detected at a greater level in the large intestine for MPS/GCZ. MPS/GCZ ameliorated TNBS-induced colitis of rats, and this therapeutic effect was superior to that of MPS and MP. Moreover, MPS/GCZ decreased the plasma levels of corticosterone and ACTH to a greater extent than MPS, but less than MP.
conclusionsCo-administration of GCZ, a reduction inhibitor, may be a plausible strategy to reduce the therapeutic loss of MP produced from MPS in the large intestine, thus improving the therapeutic property of the prodrug against inflammatory bowel disease.
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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.