ArticleDiscover oncology2026
Multi-omics unravels multiple pharmacological actions in a murine model of infantile hemangioma receiving oxymatrine therapy.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundApproximately 10% of the patients with infantile hemangioma (IH) may exhibit resistance to propranolol (PRN) therapy, and thus alternative strategies are required. Our previous studies reported that oxymatrine (OMT) could inhibit the growth of hemangiomas, however the underlying pharmacological actions have not been fully addressed.
methodsIn this study, a murine IH model was constructed by implantation of EOMA cells into nude mice. OMT was administrated (50 mg/kg; i.p) for 21 days. Metabolic changes were examined by proteomics and metabolomics, followed by in vitro experimental validation using EOMA cells.
resultsOMT significantly suppressed the growth of hemangioma in vivo without significant adverse effects. A total of 869 differentially expressed proteins and 38 metabolites were identified. In addition to canonical apoptosis regulation, OMT also caused significant metabolic disturbances, particularly in purine and pyrimidine metabolism. Furthermore, ferroptosis may be involved in the therapeutic effect of OMT. In the validation experiments in vitro, we found that OMT dose-dependently reduced the viability of EOMA cells, concomitant with increased production of lipid reactive oxygen species (ROS) and Fe2 + accumulation.
conclusionsIn conclusion, these findings suggested that treatment with OMT could suppress the growth of hemangiomas through metabolic disturbances and inducing ferroptosis, which may provide new insights to the management of IH.
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