To investigate the molecular mechanism of polysaccharide krestin (PSK) on atherosclerosis's prevention and treatment.Macrophages were cultured and treated with or without PSK initially, Macrophage apoptosis was induced by NO and oxidized low-density lipoprotein(ox-LDL), Expression of inducible nitric oxide synthase(iNOS) mRNA by Raw264.7 macrophages as assessed by RT-PCR.PSK can inhibit ox-LDL-induced macrophage apoptosis and promote NO-induced macrophages apoptosis; Raw264.7 macrophages can be induced to express iNOS mRNA when stimulated with PSK, IFN-γ and LPS in vitro, PSK can enhance the effects of IFN-γ and LPS,suppress the inhibition effects of ox-LDL.The prevention and treatment effects of PSK on atherosclerosis may be realized by inducing iNOS.%在应用云芝多糖的基础上，用NO诱导巨噬细胞凋亡，发现云芝多糖可加强NO诱导的细胞凋亡；通过RT-PCR观察诱生性一氧化氮合酶基因的表达情况，结果表明云芝多糖能诱导一氧化氮合酶基因表达，并可增强γ干扰素和脂多糖的诱导作用，提示云芝多糖在动脉粥样硬化中的防治作用是通过诱导诱生性一氧化氮合酶表达而实现的.
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