THE POLYSACCHARIDE KRESTIN PREVENTS PLAQUE-FORMATION IN EXPERIMENTALLY ATHEROSCLEROTIC RABBITS

Our previous studies showed that lipoperoxidative injury is a major ca use of the transformation of macrophages into foam cells induced by ox idatively modified low density lipoprotein (O-LDL), and that the polys accharide krestin (PSK), administered intraperitoneally to mice, enhan ced selenium-dependent glutathione peroxidase gene expression in macro phages, protected in vitro macrophages from foam cell formation caused by O-LDL and prevented lipoperoxidative injury to experimentally athe rosclerotic rabbits. The aim of the present study was to determine whe ther PSK could prevent plaque formation in experimentally atherosclero tic 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 fewer in the PSK group (28.9% vs 71.0%). Stenosis of the coronary art ery branches in the heart wall of the PSK group was also milder than i n the control group. Prevention of the transformation of macrophages i nto foam cells by elevation of their antioxidation potential may be an other important means to prevent atherosclerosis, different from that of antioxidants given to inhibit LDL oxidation.