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Atorvastatin improves plaque stability in diabetic atherosclerosis through the RAGE pathway

F Zhou1, Y Tan, X-H Chen

  • 1Department of Neurology, The Third Affiliated Hospital of Nanchang University, Nanchang, China. wuxm79@163.com.

European Review for Medical and Pharmacological Sciences
|March 7, 2018
PubMed
Abstract

Insights

Atorvastatin enhances plaque stability in diabetic atherosclerosis by reducing lipid deposition and inflammation. This study shows atorvastatin improves arterial health via the receptor for advanced glycation end products (RAGE) pathway.

Area of Science:

  • Cardiovascular Research
  • Diabetes Mellitus Research
  • Pharmacology

Background:

  • Diabetes mellitus (DM) significantly increases the risk of atherosclerosis.
  • Diabetic atherosclerosis is characterized by plaque instability, lipid deposition, and inflammation.
  • Atorvastatin is a statin drug with potential pleiotropic effects beyond lipid lowering.

Purpose of the Study:

  • To investigate the therapeutic effects of atorvastatin on atherosclerotic plaque stability in a mouse model of diabetes mellitus.
  • To elucidate the underlying mechanisms by which atorvastatin influences plaque composition and stability in diabetic atherosclerosis.

Main Methods:

  • Apolipoprotein E knockout mice were used to establish a combined model of diabetes mellitus and atherosclerosis.
  • Histological analyses (Oil red O, Masson staining) were performed to assess lipid and collagen content.
  • Immunohistochemistry and Western blotting were employed to evaluate protein expression, including smooth muscle cells, macrophages, RAGE, MCP-1, and NF-κB.
  • Serum biomarkers such as AGEs, sRAGE, MDA, and GSH were measured.

Main Results:

  • Atorvastatin treatment significantly reduced atherosclerotic plaque area and improved plaque stability.
  • Key improvements included decreased lipid deposition, reduced macrophage and smooth muscle cell infiltration, and increased collagen content.
  • Atorvastatin administration led to decreased serum levels of advanced glycation end products (AGEs) and soluble receptor for advanced glycation end products (sRAGE).
  • The drug inhibited the RAGE signaling pathway and reduced oxidative stress markers.

Conclusions:

  • Atorvastatin effectively improves plaque stability in the context of diabetic atherosclerosis.
  • The beneficial effects are mediated, at least in part, through modulation of the receptor for advanced glycation end products (RAGE) pathway.
  • Atorvastatin's action involves reducing lipid accumulation, inflammation, and oxidative stress, thereby stabilizing atherosclerotic lesions.

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