Probucol inhibits the initiation of atherosclerosis in cholesterol-fed rabbits

Lipids Health Dis. 2013 Nov 4:12:166. doi: 10.1186/1476-511X-12-166.

Abstract

Background: Probucol and statin are often prescribed for treating atherosclerosis. These two drugs exhibit different mechanisms but it is unknown whether they have the same anti-atherogenic properties. In the current study, we examined whether these two drugs at optimal doses could inhibit the initiation of atherosclerosis in cholesterol-fed rabbits in the same way.

Methods: New Zealand White rabbits were fed a cholesterol-rich diet for 5 weeks to produce the early-stage lesions of atherosclerosis. Drug-treated rabbits were administered either probucol or atorvastatin and serum lipids and aortic atherosclerotic lesions were compared with those in a control group.

Results: Atorvastatin treatment significantly reduced serum total cholesterol levels while probucol treatment led to significant reduction of high-density lipoprotein cholesterol levels without changing total cholesterol levels compared with those in the control group. Compared with the control, probucol treatment led to 65% (p < 0.01) reduction while atorvastatin treatment led to 23% (p = 0.426) reduction of the aortic lesion area. Histological and immunohistochemical analyses revealed that the lesions of the probucol-treated group were characterized by remarkable reduction of monocyte adherence to endothelial cells and macrophage accumulation in the intima compared with those of both atorvastatin and control groups. Furthermore, low-density lipoprotein (LDL) isolated from the probucol group exhibited prominent anti-oxidative reaction, which was not present in LDL isolated from either the atorvastatin-treated or the control group.

Conclusions: This study suggests that probucol inhibits the initiation of atherosclerosis by reducing monocyte adherence and infiltration into the subintima. Anti-oxidization of LDL by probucol protects more effectively against early-stage lesion formation than statin-mediated lipid-lowering effects.

MeSH terms

  • Animals
  • Anticholesteremic Agents / pharmacology*
  • Aorta / drug effects
  • Aorta / pathology
  • Atherosclerosis / blood
  • Atherosclerosis / etiology
  • Atherosclerosis / prevention & control*
  • Atorvastatin
  • Cell Adhesion / drug effects
  • Cholesterol / adverse effects
  • Cholesterol / blood
  • Cholesterol, HDL / blood
  • Cholesterol, LDL / blood*
  • Dietary Fats / adverse effects
  • Dietary Fats / blood
  • Endothelial Cells / drug effects
  • Endothelial Cells / pathology
  • Heptanoic Acids / pharmacology
  • Hypercholesterolemia / blood
  • Hypercholesterolemia / etiology
  • Hypercholesterolemia / prevention & control*
  • Macrophages / drug effects
  • Macrophages / pathology
  • Male
  • Monocytes / drug effects
  • Monocytes / pathology
  • Plaque, Atherosclerotic / pathology
  • Plaque, Atherosclerotic / prevention & control*
  • Probucol / pharmacology*
  • Pyrroles / pharmacology
  • Rabbits
  • Triglycerides / blood
  • Tunica Intima / drug effects
  • Tunica Intima / pathology

Substances

  • Anticholesteremic Agents
  • Cholesterol, HDL
  • Cholesterol, LDL
  • Dietary Fats
  • Heptanoic Acids
  • Pyrroles
  • Triglycerides
  • Cholesterol
  • Atorvastatin
  • Probucol