Effect of Hesperetin on Isoprenaline-induced Hypertrophy of H9C2 Cardiomyocytes

Bo Liu1, Beilei Qiu1, Suchuan Zhang1

  • 1Department of Cardiology, Wuhan Sixth Hospital (Affiliated Hospital of Jianghan University), Wuhan, 430016, Hubei Province, China. zhangsuchuan2022@yandex.com.

Insights

Hesperetin effectively reduces isoproterenol-induced H9C2 cardiomyocyte hypertrophy by decreasing beta-MHC mRNA and increasing autophagy marker LC3II expression. This suggests hesperetin may improve cardiac hypertrophy by activating autophagy.

Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Pharmacology

Background:

  • Cardiac hypertrophy is a significant risk factor for heart failure.
  • Isoproterenol is commonly used to induce experimental models of cardiac hypertrophy.
  • Hesperetin, a flavonoid, has shown potential cardioprotective effects.

Purpose of the Study:

  • To investigate the effect of hesperetin on isoproterenol-induced H9C2 cardiomyocyte hypertrophy.
  • To elucidate the underlying mechanism involving autophagy.

Main Methods:

  • H9C2 cardiomyocytes were treated with isoproterenol and varying concentrations of hesperetin.
  • Cell area, beta-myosin heavy chain (β-MHC) mRNA expression, and microtubule-associated protein 1A/1B-light chain 3 II (LC3II) expression were measured.
  • Time-course experiments were conducted to assess the effects of hesperetin over 6, 12, and 24 hours.

Main Results:

  • Hesperetin significantly reduced the isoproterenol-induced increase in H9C2 cardiomyocyte area.
  • Hesperetin decreased the expression of the cardiac hypertrophy marker β-MHC mRNA.
  • Hesperetin treatment led to an increased expression level of the autophagy marker LC3II.

Conclusions:

  • Hesperetin demonstrates a protective effect against isoproterenol-induced cardiac hypertrophy in H9C2 cells.
  • The mechanism of hesperetin's action may involve the activation of autophagy.
  • Hesperetin shows potential as a therapeutic agent for managing cardiac hypertrophy.

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