一氧化氮在低密度脂蛋白氧化中的作用及调控研究  

Effects and Regulation Mechanism of Nitric Oxide on Oxidation of Low Density Lipoprotein

作　　者：王瑾雯 陈瑗 周玫 

机构地区：[1]第一军医大学生物化学与分子生物学研究所,广州510515

出　　处：《中国动脉硬化杂志》1999年第3期222-224,共3页Chinese Journal of Arteriosclerosis

摘　　要：通过给小鼠腹腔注射云芝多糖，并用干扰素γ、脂多糖及佛波酯醇刺激细胞，观察细胞一氧化氮的产量，测定脂氢过氧化物和硫代巴比妥酸反应物质，以反应低密度脂蛋白的氧化程度，从而部分揭示巨噬细胞氧化低密度脂蛋白的机制，探讨一氧化氮在低密度脂蛋白氧化中的作用和云芝多糖的抑制效果。结果显示，干扰素γ和脂多糖及云芝多糖均可增加一氧化氮的释放量（ Ｐ＜ ０ ．０５） ，减轻低密度脂蛋白的氧化（ Ｐ＜ ０ ．０５） ，佛波酯醇的作用则相反。表明干扰素γ和脂多糖及云芝多糖可能通过诱导细胞诱生性一氧化氮合酶的活性，产生大量的一氧化氮，从而保护细胞，抑制低密度脂蛋白的氧化。Aim Effects of nitric oxide (NO),superoxide anion(O . 2 ) and polysaccharide krestin(PSK) on macrophage-mediated oxidation of LDL were investigated. Methods Mouse were given peritoneal injection PSK (control mouse were given injection physiological saline), peritoneal macrophages were collected and stimulated with low-density lipoprotein(LDL), γ-IFN, LPS and PMA. Contents change of nitrite, hydroperoxides and TBARS were measured. Results PSK-treated mouse peritoneal macrophages secreted much NO and produced less LOOH, TBARS than non-PSK-treated. Much NO and less LOOH, TBARS could be found to be produced by macrophage when stimulated with γ-IFN, LPS, macrophages stimulated with PMA appeared opposite effect. Conclusions The results indicated PSK has a protective effect, prevent cell from lipoperoxidative injury. γ-IFN and LPS could induce NO synthase activity and produce substantial NO. Stimulated macrophages were less efficient in oxidizing LDL. PMA can activate the respiratory burst, the stimulated cells were more effective than unstimulated cells in modifying LDL, and that O - 2 was of critical importance.

关 键 词：云芝多糖 干扰素 佛波酯醇 低密度脂蛋白 

分 类 号：R285.5[医药卫生—中药学]