The effect of polysaccharide krestin on nitric oxide production in mouse peritoneal macrophages

Abstract

Nitric oxide (NO) has an important role in preventing vascular thrombosis, inflammatory cell-mediated injury and reperfusion injury. It can inhibit several components of the atherogenic process. Polysaccharide krestin (PSK) is a protein-bound polysaccharide with proven effects on tumour therapy. Our previous work showed that PSK could protect macrophages from oxidative injury and prevent atherosclerosis. In order to determine the mechanisms of PSK action, we have now studied its effect on NO production in mouse peritoneal macrophages. The content of NO in cell cultures was analysed using Griess reagent, and the cell number determined by staining with crystal violet. There was no alteration in NO production by PSK-primed mouse peritoneal macrophages without any stimulation; but when the cells were stimulated with lipopolysaccharide (LPS), NO production increased significantly, Furthermore, NO production did not change when the PSK-primed macrophages were incubated with interferon-γ (IFN-γ). PSK may possibly exert its anti-atherogenic effects partly through regulating NO production in macrophages. The effect of PSK was similar to that of IFN-γ. The relationship between the effects of PSK and IFN-γ needs to be uncovered.