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<p>Doxorubicin (DOX) is a commonly prescribed chemotherapeutic regimen, but its practice is challenged by cardiotoxicity risks. Herbacetin (HBT), a bioactive flavonoid compound, has demonstrated anti-oxidative, anti-inflammation, and anti-tumor properties. This study aimed to evaluate the protective effects of HBT against DOX cardiotoxicity along with the underlying mechanisms. In vitro, HBT enhanced cell survival, prevented DNA damage, reduced mitochondrial ROS, and maintained mitochondrial integrity in DOX-treated cardiomyocytes. Using an acute DOX cardiotoxicity rat model, HBT prevented DOX-induced declined cardiac function and reversed cardiac remodeling depicted by increased cell size. RNA sequence analysis of PBS-, DOX-, and DOX + HBT-treated H9c2 cardiomyocytes suggested the involvement of the MAPK signaling pathway in cardioprotective effects of HBT. Specifically, the level of phosphorylated ERK1/2 was increased in DOX-treated cardiomyocytes, which declined in the presence of HBT. The decreased level of FOXO3a (downstream factor of ERK1/2) by DOX was further restored by HBT. Lastly, the knockdown of FOXO3a abrogated the cardioprotective benefits of HBT. Our data suggest that HBT mitigates acute DOX cardiotoxicity via regulating the ERK1/2-FOXO3a signaling pathway, highlighting its potential as a novel therapeutic agent against DOX cardiotoxicity.</p> Graphical abstract <p></p>

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Herbacetin alleviates acute doxorubicin cardiotoxicity via regulating the ERK1/2-FOXO3a signaling pathway

  • 期刊论文

  • 发表日期：

    2026年3月3日

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  • Sijia Bian,
  • Xinran Li,
  • Peiyan Zhu,
  • Zhiting Jiang,
  • Chen Yan,
  • Shuling Wei,
  • Liqi Luo,
  • Yuhua Zhu,
  • Lan Luo

摘要

Doxorubicin (DOX) is a commonly prescribed chemotherapeutic regimen, but its practice is challenged by cardiotoxicity risks. Herbacetin (HBT), a bioactive flavonoid compound, has demonstrated anti-oxidative, anti-inflammation, and anti-tumor properties. This study aimed to evaluate the protective effects of HBT against DOX cardiotoxicity along with the underlying mechanisms. In vitro, HBT enhanced cell survival, prevented DNA damage, reduced mitochondrial ROS, and maintained mitochondrial integrity in DOX-treated cardiomyocytes. Using an acute DOX cardiotoxicity rat model, HBT prevented DOX-induced declined cardiac function and reversed cardiac remodeling depicted by increased cell size. RNA sequence analysis of PBS-, DOX-, and DOX + HBT-treated H9c2 cardiomyocytes suggested the involvement of the MAPK signaling pathway in cardioprotective effects of HBT. Specifically, the level of phosphorylated ERK1/2 was increased in DOX-treated cardiomyocytes, which declined in the presence of HBT. The decreased level of FOXO3a (downstream factor of ERK1/2) by DOX was further restored by HBT. Lastly, the knockdown of FOXO3a abrogated the cardioprotective benefits of HBT. Our data suggest that HBT mitigates acute DOX cardiotoxicity via regulating the ERK1/2-FOXO3a signaling pathway, highlighting its potential as a novel therapeutic agent against DOX cardiotoxicity.

Graphical abstract