摘要
目的 :观察人脐静脉内皮细胞 (HUVEC)在氧化型低密度脂蛋白 (ox LDL)作用下内皮源性一氧化氮合酶 (eNOS)和细胞间黏附分子 1(ICAM 1)的变化及血脂康的干预作用。方法 :体外培养HUVEC ,制备ox LDL。用不同浓度 (5 0、10 0、2 0 0mg/L)的ox LDL和血脂康 (0 .1、0 .2 g/L)分别作用于HUVEC。 2 4h后 ,测定各组和对照组的eNOS和ICAM 1的含量 ;用免疫组化技术和图像分析法观察eNOS表达的变化 ;用酶联免疫吸附法测定细胞表面表达的黏附分子。结果 :ox LDL能抑制HUVEC产生的NOS活性和增强HUVEC产生的I CAM 1含量 ,与对照组比较差异均有统计学意义 ,且随ox LDL浓度增加 ,NOS活性减低呈剂量依赖性效应。血脂康能刺激HUVEC产生的NOS活性和减少ICAM 1的产生 ,与对照组比较差异均有统计学意义。结论 :ox LDL使HUVEC的NOS活性下降及ICAM 1增强 ,这对动脉粥样硬化 (AS)的发生起一定的作用。血脂康使HU VEC的NOS活性增强并减少ICAM 1的产生 ,对防治AS的发生起一定的作用。
Objective:To investigate the effects of oxidized low density lipoprotein (ox-LDL) and xuezhikang on nitric oxide synthase (NOS) activity and intercellular adhesion molecule-1 (ICAM-1) in cultured human umbilical vein endothelial cells (HUVEC).Method:HUVECS were cultured in vitro. The HUVECs were subjected to different concentrations of ox-LDL (50, 100, 200 mg/L) and different concentrations of xuezhikang ( 0.1, 0.2 g/L) for 24 h. The level of NOS and ICAM-1 in the HUVECs was determined . The level of NOS activity was measured with immunohistochemistry technique and image analyzing method. The level of ICAM-1 was measured with cell-ELISA.Result:ox-LDL significantly decreases NOS activity in a dose dependent manner and increases ICAM-1 expression in HUVEC. Xuezhikang increases NOS activity and decreases ICAM-1 expression in HUVEC.Conclusion:ox-LDL decreases NOS activity and increases ICAM-1 exprossion in HUVEC. Thus ox-LDL may play an important role in the genesis and development of atherosclorosis.Xuezhikang increases NOS activity and dcereases ICAM-1 expression. So xuezhikang may play an important role in preventing the genesis and development of atherosclerosis.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2004年第6期355-357,共3页
Journal of Clinical Cardiology
