The polysaccharide krestin prevents lipoperoxidative injury to experimentally atherosclerotic rabbits

Abstract

There is a close relationship between the development of atherosclerosis and oxidative modification of low density lipoprotein (O-LDL). Macrophage-derived foam cell formation is one of the early important pathological lesions in atherogenesis. Our previous studies have shown that lipoperoxidative injury is a major cause of transformation of macrophages into foam cells induced by O-LDL, and that polysaccharide krestin (PSK), administrated intraperitoneally to mice, could enhance selenium-dependent glutathione peroxidase (SeGSHPx) gene expression of macrophage and protect in vitro macrophage from foam cell formation caused by O-LDL. The present results show that PSK can prevent lipoperoxidative injury to the experimental atherosclerotic rabbits. The lipoperoxide (LPO) levels in the plasma, LDL and tissues (aorta, heart and liver) were much lower and the SeGSHPx activities, and especially the SeGSHPx/LPO ratios were much higher in the PSK group as compared with those in the control group. The results show that prevention of transformation of macrophages into foam cells by elevation of their antioxidation potential may be another important means of preventing the development of atherosclerosis.