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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 observe the changes of endothelial nitric oxide synthase (eNOS) and intercellular adhesion molecule-1 (ICAM 1) in human umbilical vein endothelial cells (HUVECs) induced by ox-LDL and the effects of Xuezhikang The role of intervention. Methods: HUVECs were cultured in vitro to prepare ox LDL. HUVECs were treated with different doses of ox LDL and Xuezhikang (0.1,0.2 g / L) at different concentrations (50, 100, 200 mg / L). After 24 hours, the content of eNOS and ICAM 1 in each group and the control group were determined. The changes of eNOS expression were observed by immunohistochemistry and image analysis. The adhesion molecules expressed on the cell surface were measured by enzyme-linked immunosorbent assay. RESULTS: Ox LDL could inhibit the activity of NOS produced by HUVEC and increase the content of I CAM 1 produced by HUVEC. Compared with the control group, ox LDL had statistical significance. With the increase of ox LDL concentration, the activity of NOS decreased in a dose-dependent manner. Xuezhikang can stimulate the production of NOS HUVEC activity and reduce the production of ICAM 1, compared with the control group differences were statistically significant. CONCLUSION: ox LDL decreases the activity of NOS in HUVEC and enhances ICAM-1, which plays a role in the pathogenesis of atherosclerosis (AS). Xuezhikang HU VEC increased NOS activity and reduce the production of ICAM 1, play a role in the prevention and treatment of AS.