腹腔注射云芝多糖对小鼠腹腔巨噬细胞一氧化氮产生的影响  

Nitric Oxide Production in Mouse Peritoneal Macrophages Primed by Polysaccharide Krestin Injected Peritoneally

作　　者：庞战军[1] 陈瑗[1] 周玫[1] 

机构地区：[1]第一军医大学自由基医学研究室

出　　处：《中国动脉硬化杂志》1999年第2期155-157,共3页Chinese Journal of Arteriosclerosis

摘　　要：为探讨云芝多糖对巨噬细胞一氧化氮产生的影响，采用Ｇｒｉｅｓ试剂法对小鼠腹腔巨噬细胞培养上清液中一氧化氮的含量进行测定，并用结晶紫染核法测定细胞数目。结果发现，在不受任何刺激的情况下，云芝多糖活化的巨噬细胞一氧化氮的释放并不增加；而在脂多糖作用下，其一氧化氮产量明显增加；云芝多糖活化的巨噬细胞与γ干扰素共孵，并未见一氧化氮产量增加。提示云芝多糖对巨噬细胞的激活采用的方式与γ干扰素类似，其抗动脉粥样硬化的效应可能部分源自于其对巨噬细胞一氧化氮生成的调节。Aim In order to find out the effect of polysaccharide krestin(PSK) on nitric oxide (NO) production in mouse peritoneal macrophages. Methods The content of NO in cell cultures was analyzed by a method using Griess reagent, and the cell number was determined by staining with crystal violet. Results Without any stimulation,there was no alteration of NO production in mouse peritoneal macrophages by PSK primed, but when the cells were stimulated with lipopolysaccharide (LPS), NO production increased greatly(P< 0.01 ); furthermore, NO production didn't change when the PSK primed macrophages were incubated with interferon γ (IFN γ). Conclusion PSK could regulate NO production in macrophages; and the effect of PSK was somewhat like that of IFN γ. The relationship between the effects of PSK and IFN γ needs to be further uncovered.

关 键 词：云芝多糖 一氧化氮 巨噬细胞活化 

分 类 号：R285.5[医药卫生—中药学]