Ononin alleviates H2O2-induced cardiomyocyte apoptosis and improves cardiac function by activating the

Rongrong Pan1, Qin Zhuang1, Jiangtin Wang2

  • 1Department of Cardiology, Cixi People's Hospital, Wenzhou Medical University, Cixi, Zhejiang 315300, P.R. China.

Insights

Ononin protects heart cells from injury by enhancing autophagy, a cellular recycling process. This isoflavone activates the AMPK/mTOR pathway, reducing apoptosis and improving heart function in myocardial infarction models.

Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanisms
  • Pharmacology

Background:

  • Ononin (ON) is an isoflavone with known bioactivities.
  • Autophagy is crucial for cardiomyocyte homeostasis and linked to apoptosis.
  • Understanding ON's cardioprotective mechanisms is vital.

Purpose of the Study:

  • To investigate the effects of Ononin (ON) on H2O2-induced cardiomyocyte apoptosis and myocardial infarction.
  • To elucidate the underlying molecular mechanisms, focusing on autophagy and the AMPK/mTOR pathway.

Main Methods:

  • In vitro studies using H9C2 cells treated with H2O2 and ON.
  • Flow cytometry and western blotting to assess apoptosis and autophagy markers.
  • In vivo studies using a rat myocardial infarction model.

Main Results:

  • ON demonstrated anti-apoptotic effects by reducing cleaved-caspase 3.
  • ON enhanced autophagy, indicated by increased LC3B and p62 degradation.
  • ON activated the AMPK/mTOR pathway, crucial for its protective effects.
  • In vivo, ON improved ejection fraction and reduced cardiac fibrosis in myocardial infarction models.

Conclusions:

  • Ononin exerts significant cardioprotective effects against apoptosis and myocardial infarction.
  • These effects are mediated by the enhancement of autophagy via the AMPK/mTOR signaling pathway.
  • ON represents a potential therapeutic agent for cardiovascular diseases.

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