Effect of polysaccharide Krestin on the up-regulation of macrophage colony-stimulating factor gene expression in protecting mouse peritoneal macrophages from oxidative injury.

Oxidative injury caused by oxidatively modified low density lipoprotein (Ox-LDL) plays an important role in the transformation of macrophages into foam cells and atherogenesis. Treatments to protect macrophages from oxidative injury will be effective in treating atherosclerosis. A macrophage-specific growth factor, macrophage colony-stimulating factor (M-CSF), was reported to be able to prevent the progression of atherosclerosis in Watanabe heritable hypercholesterolemic (WHHL) rabbits. A protein-bound polysaccharide, polysaccharide Krestin (PSK), was also proven to have effects in preventing atherosclerosis in our previous work. We proposed that, both M-CSF and PSK could protect macrophages from oxidative injury, and the effects of PSK were associated with its capability of inducing M-CSF expression. In our present results, M-CSF could alleviate the Ox-LDL- or tert-butyl hydroperoxide (tbOOH)-induced injury to mouse peritoneal macrophages, and PSK exhibited some similar effects. PSK treatment could induce M-CSF gene expression and secretion in mouse peritoneal macrophages. Furthermore actinomycin D and cycloheximide could attenuate that induction. We concluded that, maybe PSK exerted its effects on macrophages partly through the transcriptional induction of M-CSF in the cells.