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DiOHF Protects Against Doxorubicin-Induced Cardiotoxicity Through ERK1 Signaling Pathway

Danqi Chang1, Hang Li1, Cheng Qian1

  • 1Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.

Frontiers in Pharmacology
|October 16, 2019
PubMed

Insights

3

Area of Science:

  • Cardiovascular Pharmacology
  • Molecular Toxicology

Background:

  • Doxorubicin (DOX) is a potent chemotherapy drug with dose-limiting cardiotoxicity.
  • Cardiotoxicity involves reactive oxygen species (ROS), mitochondrial dysfunction, and apoptosis.
  • Synthetic flavonoid 3',4'-dihydroxyflavonol (DiOHF) shows antioxidant and mitochondrial protective properties.

Purpose of the Study:

  • To investigate the protective effects of DiOHF against DOX-induced cardiotoxicity.
  • To elucidate the underlying mechanisms of DiOHF's cardioprotection.

Main Methods:

  • DOX-induced cardiotoxicity models were established in H9C2 cells and BALB/c mice.
  • Effects of DiOHF on ROS production, mitochondrial function, apoptosis, and ERK signaling were assessed.
  • Cardiac function, serum CK-MB levels, and myocardial fibrosis were evaluated in vivo.

Main Results:

  • DiOHF prevented and reversed DOX-induced cardiotoxicity in vitro and in vivo.
  • DiOHF attenuated ROS generation, mitochondrial dysfunction, and apoptosis.
  • DOX-induced cardiotoxicity involved ERK1 activation, which was crucial for the observed effects.

Conclusions:

  • DiOHF effectively protects against and reverses doxorubicin-induced cardiotoxicity.
  • Cardioprotection is mediated by inhibiting ROS, stabilizing mitochondria, and reducing apoptosis via ERK1 activation.
  • DiOHF represents a potential therapeutic strategy to mitigate chemotherapy-induced heart damage.
Keywords:
DiOHFERK1/2cardiotoxicitydoxorubicinsiRNA

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