The polysaccharide krestin prevents plaque formation in experimentally atherosclerotic rabbits

Abstract

Our previous studies showed that lipoperoxidative injury is a major cause of the transformation of macrophages into foam cells induced by oxidatively modified low density lipoprotein (O-LDL), and that the polysaccharide krestin (PSK), administered intraperitoneally to mice, enhanced selenium-dependent glutathione peroxidase gene expression in macrophages, protected in vitro macrophages from foam cell formation caused by O-LDL and prevented lipoperoxidative injury to experimentally atherosclerotic rabbits. The aim of the present study was to determine whether PSK could prevent plaque formation in experimentally atherosclerotic rabbits. The plaque area of the aorta in a given PSK group was 69.9% lower than in the control group. The percentage of plaque formation at the opening of arteries in the abdominal aorta was relatively much lower in the PSK group (28.9% vs 71.0%). Stenosis of the coronary artery branches in the heart wall of the PSK group was also milder than in the control group. Prevention of the transformation of macrophages into foam cells by elevation of their antioxidation potential may be another important means to prevent atherosclerosis, different from that of antioxidants given to inhibit LDL oxidation.