云芝多糖对氧化修饰LDL抑制巨噬细胞一氧化氮产生的保护作用  

Protective effect of PSK on the inhibition of lipopolysaccharide-induced nitric oxide production in macrophages by oxidized low density lipoprotein

作　　者：刘尚喜[1] 周玫[1] 陈瑗[1] 

机构地区：[1]第一军医大学自由基医学研究室,广州510515

出　　处：《第一军医大学学报》1998年第1期4-7,共4页Journal of First Military Medical University

基　　金：国家自然科学基金

摘　　要：通过测定巨噬细胞培养上清液中亚硝酸盐的含量和观察细胞内一氧化氮合酶（NOS）mRNA含量的变化，研究了云芝多糖（PSK）对氧化修饰LDL（Ox－LDL）抑制脂多糖（LPS）诱导的巨噬细胞NO产生的保护作用。结果显示，Ox－LDL可抑制LPS诱导的巨噬细胞NO产生，而正常（N－LDL）和乙酰化LDL（AC－LDL）则没有抑制作用。非特异性免疫调节剂PSK处理小鼠对Ox－LDL引起的巨噬细胞NO产生量下降具有保护作用。狭缝杂交结果显示，Ox－LDL可使LPS诱导的巨噬细胞NOSmRNA含量下降，PSK可保护巨噬细胞免受Ox－LDL引起的NOSmRNA含量下降。Protective effect of Polysaccharide Krestin (PSK) on the inhibition of lipopolysaccharide (LPS)-stimu1ated nitric oxide(NO) production in macrophages caused by oxidized low density lipoprotein (Ox-LDL) was studied by measuring nitrite in the media and mRNA for NOS in the macrophages. The results showed that exposure of mouse peritoneal macrophages to Ox-LDL could inhibit NO production stimulated by LPS, meanwhile native LDL and acetylated LDL could not. PSK, peri toneally injected into mice,could protect their macrophages from'the inhibition of NO production caused by Ox-LDL. Results obtained from slot hybridization showed that Ox-LDL could decrease the content of mRNA for NOS in macrophages induced by LPS and PSK could protect macrophages from the decrease of that caused by Ox-LDL.

关 键 词：氧化修饰 LDL 云芝多糖 巨噬细胞 一氧化氮 

分 类 号：R979.5[医药卫生—药品] R977.6[医药卫生—药学]