In spite of this, Kyolic reduced by 64% (P < 0.05) the surface area of the thoracic aorta covered by fatty streaks and significantly reduced aortic arch cholesterol. Kyolic also significantly inhibited by ∼50% the development of thickened, lipid-filled lesions in preformed neointimas produced by Fogarty 2F balloon catheter injury of the right carotid artery in cholesterol-fed rabbits. In vitro studies found that Kyolic completely prevented vascular smooth muscle phenotypic change from the contractile, high volume fraction of filament (Vvmyo) state, and inhibited proliferation of smooth muscle cells in the synthetic state with a 50% effective dose (ED50) of 0.2%.
Kyolic also slightly inhibited the accumulation of lipid in cultured macrophages but not smooth muscle, and had no effect on the expression of adhesion molecules on the surface of the endothelium or the adherence of leukocytes. It is concluded that Kyolic exerts antiatherogenic effects through inhibition of smooth muscle phenotypic change and proliferation, and by another (unclarified) effect on lipid accumulation in the artery wall.
Extracts of garlic are known to reduce serum cholesterol levels in humans, inhibit cholesterol biosynthesis, suppress LDL oxidation, lower plasma fibrinogen and increase fibrinolytic activity (Bordia et al. 1977, Harenberg et al. 1988), and thus to possess antiatherosclerotic properties (Lau et al. 1987, Phelps and Harris 1993). However, atherosclerosis is a complex disease, which can be described as an excessive inflammatory, fibro-fatty, proliferative response to damage of the artery wall involving several cell types, particularly smooth muscle cells (SMC),3monocyte-derived macrophages, T-lymphocytes and platelets (Schwartz et al. 1993). Many people believe it can be induced from simple dysfunction of the endothelial lining as occurs with hyperlipidemia, hypertension or cigarette smoke, causing imbalance of angiotensin II and nitric oxide production in the artery wall (Dusting et al. 1998, Luscher and Noll 1995). This initiates a cascade of events, which includes expression of adhesion molecules on the surface of the endothelium, the oxidation of lipoproteins, monocyte invasion of the vessel wall, foam cell formation, smooth muscle phenotypic change, and proliferation and platelet deposition (Ross 1993).
In this study, we determined the effect of the aged garlic extract (AGE) Kyolic (Wakunaga Company, Mission Viejo, CA) on the development of atherosclerosis in a rabbit model of the disease as an extension of our earlier report (Efendy et al. 1997), and examined how it might function at a cellular and molecular level using cell culture techniques.
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