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Atorvastatin alleviates left ventricular remodeling in isoproterenol-induced chronic heart failure in rats by

Dingjun Sun1, Fuwei Zhang1, Tianyi Ma1

  • 1Department of Cardiology, Central South University Xiangya School of Medicine Affiliated Haikou Hospital (Haikou People's Hospital), Haikou, 570208, People's Republic of China.

Pharmacological Reports : PR
|March 8, 2020
PubMed

Insights

Atorvastatin treatment improved cardiac function and reduced left ventricular remodeling in rats with chronic heart failure (CHF). This was achieved by inhibiting the RhoA/Rho kinase signaling pathway, suggesting a novel therapeutic mechanism for CHF.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Chronic heart failure (CHF) involves left ventricular dysfunction and impaired autonomic cardiac control.
  • Isoproterenol-induced rat models are used to study CHF mechanisms.

Purpose of the Study:

  • To investigate atorvastatin's effects on left ventricular remodeling (LVR) and cardiac function in a rat model of isoproterenol-induced CHF.
  • To elucidate the underlying mechanism involving the RhoA/Rho kinase signaling pathway.

Main Methods:

  • Rats with isoproterenol-induced CHF were treated with atorvastatin.
  • Assessed cardiac function and LVR using echocardiography and hemodynamic measurements.
  • Quantified gene and protein expression of key signaling molecules (RhoA, Rho kinase, eNOS) and oxidative stress markers (NADPH oxidase, ROS, NO) via RT-qPCR, Western blot, and ELISA.

Main Results:

  • Atorvastatin treatment significantly improved cardiac function, indicated by increased fractional shortening and ejection pressure, and reduced ventricular dimensions and pressures.
  • Atorvastatin decreased the expression of RhoA, Rho kinase, and myosin-binding subunit (MBS), while increasing endothelial nitric oxide synthase (eNOS) expression.
  • Reduced activity of NADPH oxidase and reactive oxygen species (ROS) was observed, alongside decreased nitric oxide (NO) levels.

Conclusions:

  • Atorvastatin effectively inhibits left ventricular remodeling and enhances cardiac function in a rat model of CHF.
  • The therapeutic effects are mediated through the inhibition of the RhoA/Rho kinase signaling pathway and modulation of oxidative stress markers.
Abstract

Keywords:
AtorvastatinCardiac functionChronic heart failureEndothelial nitric oxide synthaseIsoproterenolLeft ventricular remodelingRhoA/Rho kinase

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