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


GÖÇMEN A. Y. , OCAK G. A. , ÖZBİLİM G., Delibas N., GÜMÜŞLÜ S.

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, vol.91, no.9, pp.680-685, 2013 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 91 Issue: 9
  • Publication Date: 2013
  • Doi Number: 10.1139/cjpp-2012-0325
  • Title of Journal : CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
  • Page Numbers: pp.680-685

Abstract

We aimed to investigate whether atorvastatin influenced the CD40-CD40L pathway in atherosclerosis formation in rats fed a high cholesterol diet. Thirty-six male Wistar rats were divided among 4 groups as follows: control (C), statin (S), 5% cholesterol fed (HC), and statin-administered hypercholesterolemic (HCS). Serum levels of lipids, soluble CD40L, platelet factor 4, and interleukin-6 were assayed with commercial kits. The number of platelets expressing surface P-selectin, CD40, and CD40L were determined by flow cytometry. Aortas were examined for fatty streaks. In the HC group, we observed a significant increase in serum lipid levels and platelet activation markers compared with the control group. Rats in the HCS group had a significant decrease in lipid levels and downregulation in the number of platelets expressing surface P-selectin, CD40, and CD40L compared with the HC group. We observed decreased fatty streak formations in aortas in HCS rats. A positive correlation was found for platelet activation markers and atherosclerotic fatty streak formations. Regression analysis revealed that the predictor of atherosclerosis was CD40L. Our study suggests that in a rat hypercholesterolemic model, statin treatment may influence the CD40-CD40L dyad, and that this effect is parallelled by a suppression of progression of atherosclerotic plaque formation.