ArticleBMC complementary medicine and therapies2024
Cepharanthine synergistically promotes methylprednisolone pharmacodynamics against human peripheral blood mononuclear cells possibly via regulation of P-glycoprotein/glucocorticoid receptor translocation.
Article in BMC complementary medicine and therapies, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Flow cytometric analysis of T-cell subsets and platelet surface markers in patients with immune thrombocytopenia: a case-control study.Annals of hematology · 2026Article
- Development and evaluation of cepharanthine-β-cyclodextrin inclusion complex oral tablets for prevention and treatment of COVID-19 lung injury.Scientific reports · 2025Article
- P-Glycoprotein as a Therapeutic Target in Hematological Malignancies: A Challenge to Overcome.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundCepharanthin
methodsPeripheral blood mononuclear cells (PBMCs), T lymphocytic leukemia MOLT-4 cells and daunorubicin resistant MOLT-4 cells (MOLT-4/DNR) were used to evaluate the pharmacodynamics and molecular mechanisms. Drug pharmacodynamics was evaluated by WST-8 assay. P-glycoprotein function was examined by rhodamine 123 assay. CD4
resultsCEP synergistically increased methylprednisolone (MP) efficacy with the suppressive effect on the cell viability of PBMCs. 0.3 and 1 μM of CEP significantly inhibited P-glycoprotein efflux function of CD4
conclusionsCEP synergistically promoted MP pharmacodynamics to decrease the cell viability of the mitogen-activated PBMCs, possibly via inhibiting P-glycoprotein function and potentiating GC receptor translocation. The present study provides new evidence of the therapeutic effect of Cepharanthin
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