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Updated: May 4, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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Effect of nebivolol treatment on atherosclerotic plaque components in apoE-knockout mice

G Pyka-Fosciak1, J Jawien, M Gajda

  • 1Department of Histology, Jagiellonian University Medical College, Cracow, Poland. gpfosciak@cm-uj.krakow.pl.

Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society
|January 7, 2014
PubMed

Insights

Nebivolol, a beta-blocker, was found to reduce the necrotic core and inflammatory cells within atherosclerotic plaques. This suggests nebivolol may stabilize plaques and reduce cardiovascular disease risk.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Immunology

Background:

  • Nebivolol, a third-generation beta1-blocker, has demonstrated potential in reducing atherosclerotic lesion size.
  • Atherosclerosis involves complex inflammatory processes within plaque components.

Purpose of the Study:

  • To investigate the effects of oral nebivolol on the cellular and molecular components of atherosclerotic plaques.
  • To assess nebivolol's impact on plaque stability in a mouse model.

Main Methods:

  • Utilized apoE-deficient mice, a model for atherosclerosis.
  • Administered nebivolol orally for 4 months.
  • Quantitatively evaluated plaque components using histological and immunohistochemical staining.

Main Results:

  • Nebivolol significantly decreased necrotic core area by 46% (p=0.03).
  • Reduced density of macrophages (CD68+) by 41% (p=0.008) and lymphocytes (CD3+) by 16% (p=0.03).
  • Decreased collagen content (49%, p=0.008) and matrix metalloproteinase activity (48%, p=0.008), while increasing smooth muscle content (46%, p=0.008).

Conclusions:

  • Nebivolol treatment suppresses inflammatory and immune responses within atherosclerotic plaques.
  • Nebivolol enhances plaque stability by modulating key structural and inflammatory components.

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