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Updated: Apr 26, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

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Metoprolol reduces proinflammatory cytokines and atherosclerosis in ApoE-/- mice

Marcus A Ulleryd1, Evelina Bernberg2, Li Jin Yang1

  • 1Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, P.O. Box 432, 405 30 Gothenburg, Sweden.

Biomed Research International
|August 9, 2014
PubMed

Insights

Metoprolol, a beta-blocker, reduces atherosclerosis development in mice by lowering inflammation. This study shows metoprolol

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Immunology

Background:

  • Metoprolol is a beta-1 selective adrenoceptor antagonist.
  • Previous studies suggest metoprolol may have antiatherosclerotic effects.
  • The mechanism of metoprolol's protective effect against atherosclerosis is not fully understood.

Purpose of the Study:

  • To investigate the effect of metoprolol on atherosclerosis development in apolipoprotein E-deficient (ApoE(-/-)) mice.
  • To explore metoprolol's impact on the release of proinflammatory cytokines.

Main Methods:

  • Male ApoE(-/-) mice were treated with metoprolol (2.5 mg/kg/h) or saline for 11 weeks.
  • Atherosclerosis was assessed in the thoracic aorta and aortic root.
  • Serum total cholesterol, Th1/Th2 cytokines, and macrophage content in lesions were analyzed.

Main Results:

  • Metoprolol significantly reduced atherosclerotic plaque area in the thoracic aorta.
  • Metoprolol decreased serum levels of tumor necrosis factor-alpha (TNFα) and chemokine CXCL1.
  • Macrophage content within atherosclerotic plaques was reduced by metoprolol treatment.

Conclusions:

  • Metoprolol significantly reduces atherosclerotic plaque development in ApoE(-/-) mice.
  • Metoprolol exhibits anti-inflammatory effects by decreasing proinflammatory cytokines and macrophage infiltration.
  • These findings suggest a direct antiatherosclerotic mechanism for metoprolol beyond its beta-blocking activity.

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