云芝多糖对巨噬细胞氧化LDL的抑制作用与iNOS基因表达

Effect of protein-bound polysaccharide on inhibition of LDL oxidation induced by macrophages and their relation with iNOS gene expression

目的和方法为揭示云艺多糖（PSK）的抗动脉粥样硬化机理，用RT-PCR和Westernblot等方法研究了PSK对巨噬细胞氧化低密度脂蛋白（LDL）的影响。结果PSK处理小鼠的巨噬细胞对LDL的氧化作用明显降低，NO分泌明显增加；PSK增强了IFN-Y对巨噬细胞LDL的抑制作用，减弱了一氧化氮合酶抑制剂N-Arg和DPI对细胞氧化LDL的增强作用；同时PSK能增强IFN-Y对细胞分泌NO的诱导作用，减弱N-Arg对细胞分泌NO的抑制作用；PSK能增强Raw264.7细胞iNOSmRNA和蛋白表达。结论PSK能抑制巨噬细胞对LDL的氧化，其作用机制可能与其能诱导iNOS基因表达有关。

Objective and Methods To explore the mechanism of anti-atherosclerosis of protein bound polysaccharide (PSK), theeffect of PSK on oxidation of low density lipoprotein (LDL) by macrophages were investigated using RT-PCR and Western blottechniques and by assny of contents of nitrite and hydyoperoxide. Results Ability of PSK-treated macrophage to oxidize LDL wasdecreased markedly and production of NO was increased significantly. PSK-treated macrophage could enhance the inhibition of LDLoxidation and induction of NO production by IFN- γ, alleviate the increment of LDL oxidation and inhibition of NO production by N-nitro-L-arginine and diphenylene iodonium. Meanwhile, iNOS mRNA and protein expressions induced by PSK, the expressioninduced by IFN- γ in Raw264.7 cells were enhanced by PSK. Conclusion The oxidation of LDL induced by macrophages could beinhibited by PSK, the mechanism may be related to its induction of iNOS gene expression.