摘要
为观察一氧化氮与低密度脂蛋白氧化的关系 ,揭示一氧化氮在动脉粥样硬化发病和防治中的作用 ,给小鼠腹腔注射云芝多糖 ,再用干扰素γ、脂多糖和L -精氨酸刺激小鼠腹腔巨噬细胞 ,然后检测一氧化氮释放量与脂氢过氧化物浓度。结果发现 ,一氧化氮与低密度脂蛋白氧化间有一个量的相关关系 (r =0 .75 3,P <0 .0 5 ) ,一定范围内 (≤ 5 0 μmol/L)的一氧化氮释放量与脂氢过氧化物的量呈负相关 ,即抑制细胞对低密度脂蛋白的氧化 ;当一氧化氮产生过多时 (≥ 90 μmol/L) ,脂氢过氧化物的量随之增加 ,则促进低密度脂蛋白的氧化。结果提示 ,一氧化氮在低密度脂蛋白氧化中发挥双重作用 ,它对低密度脂蛋白的氧化起抑制或促进作用取决于它的释放量。
Aim To investigate the relationship of nitric oxide (NO) and macrophage-mediated oxidation of low density lipoprotein (LDL). Methods Mice were given peritoneal injection polysaccharide krestin (PSK) (control mice were given injection physiological saline), peritoneal macrophages were collected for incubation and stimulated with LDL, interferon-γ (IFN-γ), lipopolysaccharide (LPS) and L-arginine (L-Arg). Contents of change of NO and hydroperoxides were measured. Results There is a quantity effect significance between NO and oxidation of LDL. It showed a negative correlation when the contents of NO within a certain range (approximately ≤50 μmol/L) and the contents of hydroperoxide (LOOH) decreased with that of NO increased, it meant to inhibit LDL oxidated. When the contents of NO were excessive (approximately ≥90 μmol/L) , the contents of LOOH increased with that of NO increased, it's a positive correlation and meant to promote LDL oxidated. Conclusions The results indicated there is a double effects of NO on oxidation of LDL, to inhibit or promote oxidation of LDL decided on the contents of NO.
出处
《中国动脉硬化杂志》
CAS
CSCD
2000年第4期292-294,共3页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金资助(项目编号39570867)
