摘要
为观察高密度脂蛋白是否能拮抗氧化型低密度脂蛋白对血管平滑肌细胞释放一氧化氮的抑制作用，培养了人脐动脉平滑肌细胞并用脂多糖和γ-干扰素诱导一氧化氮的释放。应用GRIESS试剂测定细胞培养基中亚硝酸盐的含量．以免疫组织化学染色和逆转录--聚合酶链反应分析诱导型一氧化氮合酶基因的表达。结果发现，氧化型低密度脂蛋白可使脂多糖和γ-干扰素诱导的平滑肌细胞一氧化氮合酶及其mRNA水平下降、抑制一氧化氮释放。而高密度脂蛋白能拮抗氧化型低密度脂蛋白对平滑队细胞释放一氧化氮的抑制作用。0．25g／L高密度脂蛋白即能显著增加一氧化氮的释放（P＜0．05），高密度脂蛋白浓度达到1．5g／L可使得一氧化氮的释放增加4．5倍。结果表明，高密度脂蛋白能提高一氧化氮合酶基因表达水平，促进一氧化氮的释放。高密度脂蛋白的作用具有浓度效应。
Aim To investigate the effect of high density lipoprotein (HDL)on the production of nitric oxide (NO)inhibited by oxidized low density lipoprotein (ox-LDL)in vascular smooth muscle cells.Methods The production of NO in cultured human vascular smooth muscle cells was analyzed by measur-ing nitrite in media with GRIESS reagent.The im-munochemical staining was used to observe the level of inducible nitric oxide synthase(iNOS).The content of mRNA for iNOS was determined by reverse tran-scription-polymerase chain reaction(RT-PCR).Results The ox-LDL could decrease the content of iNOS and level of mRNA for iNOS in vascular smooth muscle cells induced by lipopolysaccharide and inter-feron-γ,leading to inhibition of NO production.However,the addition of HDL before incubation with LDL could increase the production of NO and level of iNOS.0. 25g/L HDL could significantly increase the release of NO,and at concentration of 1.5g/L the production of NO was 4.5 limes higher than the con-trol.The effect of HDL was concentration dependent.Conclusions HDL could inhibit the activity of ox-LDL on production of NO in vascular smooth muscle cells.
出处
《中国动脉硬化杂志》
CAS
CSCD
1998年第4期292-296,共5页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金!39670796
关键词
高密度脂蛋白
一氧化氮
动脉粥样硬化
OX-LDL
High density lipoprotein
Oxidized low density lipoprotein
Nitric oxide
Atherosclerosis
