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Atorvastatin reduces cardiac and adipose tissue inflammation in rats with metabolic syndrome

Yuichiro Yamada1, Shino Takeuchi2, Mamoru Yoneda1

  • 1Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan.

International Journal of Cardiology
|May 14, 2017
PubMed

Insights

Atorvastatin reduced inflammation and fibrosis in a rat model of metabolic syndrome. These anti-inflammatory effects are linked to increased AMP-activated protein kinase (AMPK) and decreased nuclear factor-kappa B (NF-κB) activity.

Area of Science:

  • Cardiovascular Pharmacology
  • Metabolic Syndrome Research
  • Inflammation Biology

Background:

  • Statins inhibit cholesterol synthesis and prevent cardiovascular disease.
  • Statins possess cholesterol-independent anti-inflammatory effects with unclear mechanisms.
  • Metabolic syndrome (MetS) models are crucial for studying related pathologies.

Purpose of the Study:

  • To investigate atorvastatin's effects on cardiac and adipose tissue inflammation in a rat model of MetS.
  • To elucidate the molecular mechanisms behind atorvastatin's pleiotropic anti-inflammatory actions.

Main Methods:

  • DS/obese rats, a MetS model, were treated with atorvastatin (6 or 20mg/kg/day).
  • Cardiac and adipose tissue inflammation markers were assessed.
  • Gene expression of peroxisome proliferator-activated receptor γ, adiponectin levels, AMP-activated protein kinase (AMPK), and nuclear factor-kappa B (NF-κB) activities were analyzed.

Main Results:

  • Atorvastatin ameliorated cardiac fibrosis, diastolic dysfunction, oxidative stress, and inflammation.
  • Both cardiac and adipose tissue inflammation were reduced by atorvastatin at both doses.
  • Atorvastatin activated AMPK and inactivated NF-κB in the heart, while modulating these in adipose tissue.

Conclusions:

  • Atorvastatin's anti-inflammatory effects on the heart and adipose tissue in this MetS model are partly due to increased AMPK and decreased NF-κB activity.
  • These findings contribute to understanding the pleiotropic effects of statins beyond cholesterol reduction.
Abstract

Keywords:
AMP-activated protein kinaseAtorvastatinInflammationMetabolic syndromeNuclear factor–κB

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