云芝多糖对小鼠腹腔巨噬细胞NO释放及抗氧化酶活性的影响

Effect of Polysaccharide Krestin on NO production and antioxidative enzyme activity in mouse peritoneal macrophages

为探讨云芝多糖（PSK）预防动脉粥样硬化及防止氧化修饰低密度脂蛋白（O－LDL）对巨噬细胞的过氧化损伤的作用机理，考察了腹腔注射PSK对小鼠腹腔巨噬细胞谷胱甘肽过氧化物酶、超氧化物歧化酶（SOD）活性及一氧化氮（NO）释放的作用，及脂多糖（LPS）对这一作用的影响。结果显示腹腔注射PSK可以使小鼠腹腔巨噬细胞SeGSHPx酶活性、non－SeGSHPx及SOD活性升高；在LPS作用下可进一步升高上述酶活性，使NO释放量有较大增加。

In order to find out the mechanism that Polysaccharide Krestin (PSK) prevents the progression of atherosclerosis and the lipoperoxidative injury caused by oxidatively modified low density lipoprotein (OLDL) to macrophages, the alterations of GSHPx,SOD activity and NO release in PSK-treated mouse peri toneal macrophages and the effect of LPS on them were investigated. The results showed that with the peritoneal injection of PSK,the mouse peritoneal macrophages got: 1 )elevated SeGSHPx activity; 2)elevated non-SeGSHPx and SOD activity; and 3) the enzyme activity can be further improved by lipopolysaccharide (LPS); 4)much No can be found to be released by PSK-treated mouse peritoneal macrophages when stimulated with LPS.