Scholarlink

Background <p>Approximately 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.</p> Methods <p>In this study, a murine IH model was constructed by implantation of EOMA cells into nude mice. OMT was administrated (50&#xa0;mg/kg; i.p) for 21&#xa0;days. Metabolic changes were examined by proteomics and metabolomics, followed by in vitro experimental validation using EOMA cells.</p> Results <p>OMT 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.</p> Conclusions <p>In 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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Multi-omics unravels multiple pharmacological actions in a murine model of infantile hemangioma receiving oxymatrine therapy

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月1日

查看全文
  • Yang Wang,
  • Jingyu Peng,
  • Mingke Qiu,
  • Yuxin Dai,
  • Shuqing Wang,
  • Jingmin Ou,
  • Junkai Yan

摘要

Background

Approximately 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.

Methods

In 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.

Results

OMT 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.

Conclusions

In 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.