Related Experiment Video

Updated: May 8, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

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

Published on: September 26, 2018

Effect of atorvastatin on atherosclerotic plaque formation and platelet activation in hypercholesterolemic rats

Ayse Yesim Gocmen1, Guzide Ayse Ocak, Gulay Ozbilim

  • 1Department of Biochemistry, Faculty of Medicine, Bozok University, 66200 Yozgat, Turkey.

Canadian Journal of Physiology and Pharmacology
|August 30, 2013
PubMed

Insights

Atorvastatin treatment reduced atherosclerosis progression in hypercholesterolemic rats by influencing the CD40-CD40L pathway. This statin therapy decreased lipid levels and platelet activation, correlating with reduced fatty streaks.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Immunology

Background:

  • Atherosclerosis is a chronic inflammatory disease.
  • The CD40-CD40L pathway plays a role in atherogenesis.
  • Statins are widely used for cholesterol management.

Purpose of the Study:

  • To investigate the effect of atorvastatin on the CD40-CD40L pathway in a rat model of atherosclerosis.
  • To determine if atorvastatin influences platelet activation and atherosclerotic plaque formation.

Main Methods:

  • Wistar rats were divided into control, statin, high cholesterol, and statin-treated hypercholesterolemic groups.
  • Serum lipids, soluble CD40L, platelet activation markers, and interleukin-6 were measured.
  • Flow cytometry assessed platelet surface markers; aortas were examined for fatty streaks.

Main Results:

  • High cholesterol diet increased serum lipids and platelet activation.
  • Atorvastatin treatment in hypercholesterolemic rats significantly decreased lipid levels and platelet activation markers (P-selectin, CD40, CD40L).
  • Reduced fatty streak formation in aortas was observed in statin-treated hypercholesterolemic rats, with CD40L identified as a predictor of atherosclerosis.

Conclusions:

  • Atorvastatin treatment may modulate the CD40-CD40L pathway in hypercholesterolemic rats.
  • This modulation is associated with suppressed progression of atherosclerotic plaque formation.
  • The CD40-CD40L dyad is a potential therapeutic target in statin-treated atherosclerosis.

Related Concept Videos

Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Lipid-Lowering Drugs: Statins and Miscellaneous Agents01:20

Lipid-Lowering Drugs: Statins and Miscellaneous Agents

Hyperlipidemia, a medical condition often referred to as high cholesterol, is characterized by abnormally elevated levels of lipids in the bloodstream. When present in excess, these lipids, specifically cholesterol and triglycerides, can lead to serious health complications, often involving cardiovascular diseases. Illnesses like atherosclerosis, heart attacks, and pancreatitis have all been linked to untreated hyperlipidemia. This means controlling and regulating cholesterol and triglyceride...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Inflammation01:38

Inflammation

Overview
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...