低密度脂蛋白亚组份对血管细胞黏附分子-1表达的影响

背景：探讨低密度脂蛋白(LOW DENSITY LIPOPROTEIN，LDL)亚组份与人脐静脉内皮细胞(human umbilical vein endothelial cells，HUVEC)的血管细胞黏附分子-1(vascular cell adhesion molecule-1，VCAM-1)表达之间的关系，初步探讨LDL亚组份致动脉粥样硬化(atherosclerosis，AS)作用可能的分子机制。目的：观察不同LDL亚组分对HUVEC VCAM-1表达的影响。设计：随机对照的实验研究。地点和对象：本实验在北京市心肺血管疾病研究所动脉硬化研究室进行，体外培养HUVEC。干预：体外培养HUVEL，分别加入25，50，100mg／L的小而密低密度脂蛋白(small dense low-density lipoprotein，sLDL)、大而轻LDL、氧化sLDL和氧化大而轻LDL，共孵育12h和24h。主要观察指标：采用细胞表面ELISA和RT—PCR分别测定VCAM-1蛋白表达及mRNA水平。结果：HUVEC经25，50，100mg／L的sLDL刺激12h后，VCAM-1表达呈浓度依赖性明显增高(0．233&;#177;0．036，0．260&;#177;0．052，0．365&;#177;0．036，F=20．883，P&;lt;0．05)。刺激12h后，与大而轻LDL0．231&;#177;0．075。oxsLDL 0．287&;#177;0．034及氧化大而轻LDL 0．258&;#177;0．043相比，sLDL明显诱导HUVEC的VCAM-1表达(F=17．211，P&;lt;0．05)。结论：sLDL显著诱导人脐静脉内皮细胞VCAM-1的表达，可能是sLDL更易引起动脉粥样硬化的机制之一。     

2型糖尿病患者低密度脂蛋白对人脐静脉内皮细胞损伤的时间效应

目的：探讨2型糖尿病患者的低密度脂蛋白(diabetic low density lipoprotein，dLDL)损伤血管内皮细胞的机制，尤其是时间效应的影响。方法：采用人脐静脉内皮细胞(human umbilical vein endothelial cells，HUVEC)培养技术，将内皮细胞分别与正常人低密度脂蛋白native low density lipoprotein，nLDL)，dLDL，及人工氧化的低密度脂蛋白(oxidized low density lipoprotein，ox—LDL)孵育(3—48)h，观察培养上清液中一氧化氮与丙二醛的含量的变化。结果：①nLDL组的一氧化氮含量在3—24h与正常对照组相比差异无显著性意义，48h出现最大抑制，为正常对照的80％；而dLDL组与ox—LDL组在3h起就明显降低了上清液中一氧化氮的浓度，并在3h均出现最大抑制，分别为正常的62％，43％；在48h时，ox-LDL组一氧化氮含量显著上升，均值高于nLDL组，且与对照组相比差异无显著性意义。3—12h，3组LDL之间差异均有显著性意义(t=2．54—4．82，P&;lt;0．05—0．01)，24h时，dLDL与ox—LDL差异无显著性意义，48h时，3组之间差异均无显著性意义。②3组LDL均使丙二醛含量在3h就有所升高，48h时，nLDL组丙二醛含量是正常对照组的3．6倍，ox—LDL组是对照的11．6倍，而dLDL组为10．3倍。3组LDL在3—24h间差异均有显著性意义(t=3．26—14．58。P均&;lt;0．01)，而在48h时。dLDL组与ox—LDL组相比差异无显著性意义。结论：3种LDL对内皮细胞的损伤存在时间效应。     

血脂代谢紊乱与中青年脑梗死危险因素的相关性分析

目的探讨血脂与中青年人脑梗死的关系. 方法检测了 111例中青年人脑梗死患者及 80例对照者的三酰甘油、总胆固醇、高密度脂蛋白胆固醇 (High density lipoprotein cholesterol, HDL-C)、低密度脂蛋白胆固醇 (Low density lipoprotein cholesterol,LDL-C)、载脂蛋白 A-I(apolipoproteinA-I,ApoA-I)、载脂蛋白 B100(apolipoprotein B100, ApoB100)和脂蛋白 (a)血清含量. 结果脑梗死组三酰甘油 [(1.92± 1.33)mmol/L],总胆固醇 [(5.21± 1.08)mmol/L],LDL-C[(3.13± 0.96)]mmol/L,ApoB100[(1.10± 0.29)g/L]及脂蛋白 (a)[(0.23± 0.18)]g/L水平高于对照组 (t=2.523～ 3.796,P< 0.05),总胆固醇与年龄呈正相关 [青年 (4.96± 1.14)mmol/L,中年 (5.27± 1.06)mmol/L], HDL-C与年龄呈负相关 [青年 (1.39± 0.43)mmol/L,中年 (1.26± 0.35)mmol/L].亚组分析发现青年人脑梗死亚组的脂蛋白 (a)水平和中年人脑梗死亚组的三酰甘油、总胆固醇、 LDL-C、 ApoB100及脂蛋白 (a)水平均显著高于相应的对照组 (t=2.571～ 4.107,P< 0.05);皮层支动脉闭塞亚组脂蛋白 (a)水平显著高于穿通支动脉闭塞亚组 (t=5.414,P< 0.01);首发脑梗死亚组与复发脑梗死亚组之间的血脂水平无显著差异. 结论血脂代谢紊乱是中青年人脑梗死的危险因素.     

小而密低密度脂蛋白对内皮细胞间黏附分子表达的影响

目的 探讨小而密低密度脂蛋白(sLDL)致动脉粥样硬化(AS)的可能机制。方法 两步超速离心法提取人sLDL作为试验组，与培养的人脐静脉内皮细胞共同孵育12h。设置大而轻LDL、氧化sLDL、氧化大而轻LDL对照组。用酶联免疫吸附试验(ELISA)测定各组孵育细胞内皮细胞细胞间黏附分子-1(ICAM-1)的蛋白表达。同时用逆转录-聚合酶链反应(RT-PCR)检测孵育细胞ICAM-1基因表达，以磷酸甘油醛脱氢酶基因(GAPDH)扩增产物作为内对照。结果 与其他对照组比较，sLDL显著诱导培养细胞的ICAM-1信使核糖核酸(mRNA)和蛋白表达。结论 sLDL对内皮细胞功能的有较强的损伤作用，与AS的发生关系密切。     

与人脐动脉平滑肌细胞共培养的人脐静脉内皮细胞的生物学特性

目的:通过共培养人脐静脉内皮细胞(human umbilical venous endothelial ceils,HUVEC)与人脐动脉平滑肌细胞(hunlan umbilical arterial smooth muscle cells,HUASMC),初步探讨观察共培养的HUVEC的形态和增殖特性及经皮冠状动脉成形术(percutaneous transluminal coronary angioplasty,PTCA)后再狭窄的机制。 方法:用共培养装置将体外同时培养在一个培养孔中的HUVEC和HUASMC分离。在倒置显微镜下观察单独培养和共培养HUVEC的生长状态和形态;采用免疫荧光法标记细胞,流式细胞仪测定荧光强度和细胞周期。 结果:共培养的HUVEC逐渐转变为长梭形;单独培养的HUVEC仍保持鹅卵石样。单独培养的和共培养的HUVEC处于细胞周期GO/G1期和G_2+s期的百分率为:(70±3)％和(81±5)％:(22±4)％和(14± 4)％。二者均有Cyclin D的表达,但后者的表达显著低于前者。结论:共培养的HUVEC低血清干预48h形态逐渐变为长梭形,更接近于在体形状;而单独培养的HUVEC仍保持原鹅卵石状。此外,前者的增殖活性也显著低于后者。     

小密低密度脂蛋白与冠状动脉损伤严重程度的关系

目的:探讨冠心病患者小密低密度脂蛋白(small dense low-density lipoprotein,sLDL)水平与冠状动脉损伤严重程度的关系。方法:将276例接受冠状动脉造影检查的患者根据是否有主要冠状动脉或(和)其主要分支直径狭窄≥50%的情况分为对照组及冠心病组,计算所有受试者的冠状动脉损伤严重程度积分(Gensini积分),并测定其血浆中sLDL在低密度脂蛋白(low density lipoprotein,LDL)中所占的百分率。结果:冠心病组血浆sLDL水平明显高于对照组(P<0.01),sLDL与Gensini积分呈正相关(r=0.423,P<0.01)。结论:sLDL是冠心病发病的一个独立危险因素,并且与冠状动脉损伤严重程度呈正相关。     

余甘子对动脉粥样硬化家兔血浆总抗氧化能力及丙二醛和内皮素1水平的影响

背景余甘子含有丰富的维生素C、有机酸及矿物质.现代研究表明,余甘子还含有防癌、抗衰老等功效.近年来,对余甘子功能因子的研究及其相应功能食品的开发越来越引起重视.其降脂作用及其体外抗氧化作用已得到证实,但尚缺乏足够的基础研究支持.目的探讨余甘子提高高脂血症家兔机体抗氧化能力及保护血管内皮功能作用及其机制.设计以实验动物为研究对象的随机对照的实验研究.单位一所大学医院的动脉硬化实验室.材料健康新西兰家兔24只,雄性,体质量(2.2±0.5)kg.方法实验于2001-09/2002-05在北京市安贞医院动脉硬化实验室完成.将24只新西兰雄性白兔随机分为对照组、余甘子粉组(4 g/kg·d)和高胆固醇血症模型组,每组8只,余甘子和高胆固醇组实验期间均饲以高胆固醇饮食.采用酶法测定血清脂质含量;化学法测定血浆总抗氧化能力和丙二醛含量;放免法测定血浆内皮素-1含量;地高辛标记探针,组织原位杂交检测主动脉内膜内皮素mRNA表达;图象分析法测定主动脉内膜粥样硬化斑块面积,和内膜面积与中膜面积比值.主要观察指标主要结局为家兔血脂水平,血清丙二醛浓度,及动脉斑块面积比较.次要结局为血浆内皮素-1的变化.结果实验8周后余甘子果粉组与高脂组相比,①血清总胆固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)、低密度脂蛋白胆固醇(Low density lipoprotein cholesterol,LDL-C)水平显著下降[分别为(11.70±1.73),(14.32±2.22)mmol/L,P<0.05;(0.740±0.107),(1.450±0.220)mmol/L,P<0.01],血清高密度脂蛋白胆固醇(high density lipoprotein cholesterol,HDL-C)增高[(1.652±0.155),(1.179±0.142)mmol/L,P<0.01].②血浆丙二醛显著降低[(3.88±0.51),(6.29±1.43)mmol/L, P<0.01]而总抗氧化能力显著增高[(10.771±1.818),(7.350±1.158)mmol/L,P<0.05].③光镜下斑块面积、内膜面积与中膜面积比值明显降低[(39.46±6.53),(50 69±12.36)mmol/L,P<0.05;(0.62±0.32),(1.38±0.38)mmol/L,P<0.01].④血浆内皮素-1显著降低;主动脉内膜内皮素-1基因杂交阳性颗粒比高脂组明显减少.结论余甘子可能通过调整家兔脂质代谢、提高抗氧化能力减少脂质过氧化、保护内皮功能抑制动脉内膜内皮素-1基因表达而起到防止兔实验性粥样斑块的形成的作用.     

高脂血症小鼠动脉粥样硬化形成与血管内皮生长因子的关系

背景高脂血症的长期存在可促进动脉粥样硬化( atherosclerosis,AS)的形成和发展,在此过程中生长因子所起的作用越来越受重视,但对血管内皮生长因子 ( vascular endothelial growth factor, VEGF)的作用还不十分清楚.目的探讨 VEGF在 AS形成过程中的作用. 设计随机对照的实验研究. 地点、材料和干预本实验在沈阳体育学院研究生实验室完成.实验动物为 C57BL/6J(易感 AS型)纯系小黑鼠 20只.实验动物被随机分两组对照组 10只,脂肪乳组 10只.对照组喂以常备标准饲料;脂肪乳组除正常喂养外,每日以脂肪乳灌喂方式按 10 mL/kg进行高脂膳食. 主要观察指标高脂血症与非高脂血症小鼠主动脉组织光镜下形态学改变、主动脉壁的 VEGF蛋白表达、血脂水平比较. 结果对照组主动脉壁 VEGF蛋白表达均为阴性,仅外膜残存脂质 VEGF阳性.脂肪乳组血栓中、局部增生的新内膜均有 VEGF蛋白表达.血脂测定结果脂肪乳组的总胆固醇、三酰甘油、低密度脂蛋白胆固醇( low density lipoprotein cholesterol,HDL-C)分别为( 4.97± 0.10),( 2.24± 0.26),( 2.93± 0.17) mmol/L较对照组 [分别为( 4.17± 0.29),( 1.22± 0.10 ),( 2.44± 0.33) mmol/L]明显升高 (t=2.364, 2.335, 2.939, P< 0.01);脂肪乳组 HDL-C[(1.29± 0.24) mmol/L]较对照组 [(1.50± 0.16) mmol/L]明显降低 (t=2.231,P< 0.05) 结论高脂血症状态下,内源性 VEGF参与血栓形成及内膜增生,促进 AS发生发展.     

动脉粥样硬化与血管细胞黏附分子-1基因表达关系的研究

目的探讨动脉粥样硬化(AS)与血管细胞黏附分子-1(VCAM-1)基因表达的关系。方法16只大耳白兔随机分为常规饲料组(对照组)和胆固醇饲料组,饲养16周建立AS模式。饲养前后检测兔血清胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)浓度。取主动脉行病理学检查。采用免疫组化(S-P法、DAB染色)和逆转录多聚酶链式反应(PCR)方法测定主动脉壁VCAM-1阳性表达百分比和mRNA的基因表达。结果0周两组动物TC、TG、LDL差别无显著性(P>0.05),胆固醇饲料组饲养8周及16周后血清TC、LDL较0周明显升高(P<0.01),并且明显高于对照组(P<0.01)。胆固醇饲料组主动脉可见动脉粥样斑块形成,病变局部VCAM-1的阳性染色百分比和mRNA的表达量均明显高于对照组,分别为(18.38±2.55)%和(2.92±0.31)%及1.116±0.017和0.684±0.006(P<0.01)。结论AS的发生伴有VCAM-1的过度表达,这种过度表达可能与AS病变的发生发展具有一定关系。     

动态脉压与诊所脉压对原发性高血压患者左室肥厚的评估价值

目的通过比较动态脉压和诊所脉压对原发性高血压患者左室肥厚的影响,为高血压患者的康复预防和介入提供理论依据. 方法选择初诊的轻-中度原发性高血压患者 337例,所有入选病例测量非同日 3次诊所血压、进行 24 h动态血压监测和超声心动图检查.①根据动态脉压水平分为 4组、根据诊所脉压水平分为 5组并分别比较.②根据左室质量指数分为左室肥厚组和非左室肥厚组. 结果动态脉压和诊所脉压均与年龄、原发性高血压史、左室质量指数、动脉僵硬度指数和 24 h平均心率呈非常显著的相关性.动脉僵硬度随分组脉压的增大呈显著递增,其与动态脉压的相关性明显强于诊所脉压 (r=0.670,P< 0.01和 r=0.399,P< 0.01. 24 h 脉压和 24 h收缩压在左室肥厚组均明显高于非左室肥厚组 [(49.0± 10.2)mmHg 和 ( 44.7± 8.9) mmHg,P< 0.001]和 [( 132.1± 13.1) mmHg 和( 126.5± 12.7) mmHg,P< 0.001](1 mmHg=0.13 kPa);动态脉压与左室质量指数的相关性明显强于诊所脉压 (r=0.277,P< 0.01和 r=0.105,P< 0.05). 结论 脉压升高是原发性高血压患者左室肥厚的重要危险因素;与诊所脉压比较,动态脉压更能反映高血压靶器官损害的程度.     

Oxidized low-density lipoprotein increases endothelial intracellular calcium and alters cytoskeletal f-actin distribution

Central to the pathogenesis of atherosclerosis is an abnormally functioning endothelium and a consequent loss of vascular integrity. These abnormalities may be induced by haemodynamic factors, biochemical substances, and also by oxidatively modified low-density lipoprotein (LDL). To understand the mechanism by which oxidized LDL causes endothelial dysfunction, human umbilical vein endothelial cells (HUVECs) were loaded with FURA-2, and intracellular calcium mobilization was studied in acute (seconds after LDL was injected) or chronic (24 h after LDL was injected) preparations. Our results demonstrate that 100 μg mL^?1 oxidized LDL increases HUVEC intracellular calcium. In contrast, native LDL at this same concentration had no effect. In addition, chronic exposure (24 h) of HUVECs to oxidized LDL significantly increases HUVEC intracellular calcium. Fluorescent photomicrographs of HUVECs stained with BODIPY-phalloidin f-actin indicates that oxidized LDL causes a reorganization of microfilaments. The results of this study demonstrate that the mechanism by which oxidized LDL causes a loss of vascular integrity could be through activation of endothelial cells to increase cytosolic calcium, which alters the endothelial barrier by reorganizing the cytoskeleton.     

Oxidized low-density lipoprotein increases endothelial intracellular calcium and alters cytoskeletal f-actin distribution

Central to the pathogenesis of atherosclerosis is an abnormally functioning endothelium and a consequent loss of vascular integrity. These abnormalities may be induced by haemodynamic factors, biochemical substances, and also by oxidatively modified low-density lipoprotein (LDL). To understand the mechanism by which oxidized LDL causes endothelial dysfunction, human umbilical vein endothelial cells (HUVECs) were loaded with FURA-2, and intracellular calcium mobilization was studied in acute (seconds after LDL was injected) or chronic (24 h after LDL was injected) preparations. Our results demonstrate that 100 μg mL⁻¹ oxidized LDL increases HUVEC intracellular calcium. In contrast, native LDL at this same concentration had no effect. In addition, chronic exposure (24 h) of HUVECs to oxidized LDL significantly increases HUVEC intracellular calcium. Fluorescent photomicrographs of HUVECs stained with BODIPY-phalloidin f-actin indicates that oxidized LDL causes a reorganization of microfilaments. The results of this study demonstrate that the mechanism by which oxidized LDL causes a loss of vascular integrity could be through activation of endothelial cells to increase cytosolic calcium, which alters the endothelial barrier by reorganizing the cytoskeleton.     

西洛他唑对人脐静脉内皮细胞血管细胞黏附分子1和细胞间黏附分子1mRNA表达的影响

目的观察西洛他唑对人脐静脉内皮细胞（HUVECs）血管细胞黏附分子1（VCAM-1）和细胞间黏附分子1（ICAM-1）mRNA表达的影响,探讨西洛他唑可能的抗动脉粥样硬化作用机制。方法将HUVECs用不同浓度的西洛他唑（0μg/L、0.05μg/L、0.1μg/L、1.0μg/L、10μg/L）溶液处理1小时后,用肿瘤坏死因子α（TNF-α）10μg/L诱导24小时。半定量复合逆转录聚合酶链反应（RT-PCR）测定黏附分子VCAM-1和ICAM-1mRNA的表达。结果 TNF-α能上调VCAM-1和ICAM-1的表达,西洛他唑在一定程度上可抑制上述作用,随着西洛他唑浓度的增加,ICAM-1mRNA表达水平逐步下降,分别为0.239±0.012、0.205±0.012、0.166±0.010、0.136±0.008,VCAM-1mRNA表达水平也逐步下降,分别为0.114±0.048、0.093±0.051、0.083±0.045、0.068±0.039。结论西洛他唑可抑制TNF-α诱导的HUVECs的黏附分子VCAM-1和ICAM-1mRNA表达,提示西洛他唑的抗动脉粥样硬化作用可能是通过阻止血单核细胞向血管内皮细胞聚集和黏附实现的。     

Low-density lipoprotein subclass and its correlating factors in diabetics

OBJECTIVES: Small dense LDL, low density lipoprotein (LDL) particles with small size and high density, is regarded as a significant risk factor for cardiovascular diseases. Diabetes mellitus is one of the conditions accompanied by increased small dense LDL. We analyzed LDL subclass in type 2 diabetics and normal controls with LipoPrint LDL System to investigate the LDL heterogeneity in diabetics and factors affecting it. DESIGN AND METHODS: We selected 40 normal controls and 40 type 2 diabetics with fasting blood glucose level over 7.0 mmol/L and HbA1c level over 7%. LDL subclass was determined with LipoPrint LDL System. LipoPrint LDL System fractionates LDL into seven parts (LDL1-7) by size and LDL3 to LDL7 are defined as small-sized LDL. In addition we estimated 'the percent of small-sized LDL over whole LDL' and defined it as 'small-sized LDL proportion'. RESULTS: Mean small-sized LDL proportion was significantly higher in diabetics (23.4%) than in controls (11.8%) (p<0.001) and small-sized LDL proportion showed positive correlation with blood levels of glucose, HbA1c, total cholesterol, triglyceride, and oxidized LDL and negative correlation with HDL cholesterol level in univariate analysis (p<0.001). Of these parameters, triglyceride, HbA1c, oxidized LDL were statistically significant variables contributing to the small-sized LDL proportion in stepwise multiple regression analysis. CONCLUSIONS: We analyzed small-sized LDL proportion in type 2 diabetics and found that it was significantly increased in diabetics than control subjects and it was independently correlated with triglyceride, HbA1c, oxidized LDL in descending order, which are reflecting lipid metabolism, glycation, and oxidative stress, respectively.     

Circulating malondialdehyde-modified low-density lipoprotein is strongly associated with very small low-density lipoprotein cholesterol concentrations in healthy men

BACKGROUND: Despite the importance of oxidized LDL and small LDL particles as atherogenic lipoproteins, the relationship between oxidized LDL and the distributions of size subclasses of lipoproteins is not fully proved. We investigated the relationship of circulating malondialdehyde-modified (MDA)-LDL, an oxidized form of LDL, and lipoprotein subclasses in healthy men. METHODS: The study group consisted of a total of 170 healthy Japanese men (55+/-9 y). Plasma cholesterol concentrations in major lipoproteins and their subclasses were determined by HPLC with gel permeation columns. RESULTS: In univariate analysis, body mass index, waist circumference, blood pressure, white blood cell count, C-reactive protein, uric acid, fasting insulin, HOMA-IR, total cholesterol, triglycerides, each VLDL subclass cholesterol, each LDL subclass cholesterol, small HDL cholesterol, and very small HDL cholesterol were positively correlated with MDA-LDL, whereas adiponectin and large HDL cholesterol were inversely correlated with MDA-LDL. In stepwise multiple regression analysis, very small LDL cholesterol, medium VLDL cholesterol, very small HDL cholesterol, small HDL cholesterol, and systolic blood pressure were identified as independent determinants of MDA-LDL (R(2)=0.718, p<0.0001). CONCLUSIONS: Circulating MDA-LDL concentrations are strongly associated with very small LDL cholesterol concentrations in healthy men. HDL size heterogeneity has a biphasic effect on MDA-LDL.     

Sex and age differences in lipoprotein subclasses measured by nuclear magnetic resonance spectroscopy: the Framingham Study

BACKGROUND: The sex differential in coronary heart disease (CHD) risk, which is not explained by male/female differences in lipid and lipoprotein concentrations, narrows with age. We examined whether this differential CHD risk might, in part, be attributable to the sizes of lipoprotein particles or concentrations of lipoprotein subclasses. METHODS: We analyzed frozen plasma samples from 1574 men and 1692 women from exam cycle 4 (1988-1990) of the Framingham Offspring Study. Nuclear magnetic resonance (NMR) spectroscopy was used to determine the subclass concentrations and mean sizes of VLDL, LDL, and HDL particles. Concentrations of lipids and apolipoproteins were measured by standard chemical methods. RESULTS: In addition to the expected sex differences in concentrations of triglycerides, LDL-cholesterol, and HDL-cholesterol, women also had a lower-risk subclass profile consisting of larger LDL (0.4 nm) and HDL (0.5 nm) particles. The sex difference was most pronounced for HDL, with women having a twofold higher (8 vs 4 micromol/L) concentration of large HDL particles than men. Furthermore, similar to the narrowing of the sex difference in CHD risk with age, the observed male/female difference in HDL particle size also decreased with age. Although lipoprotein particle sizes were highly correlated with lipid and lipoprotein concentrations, the sex differences in the mean sizes of lipoprotein particles persisted (P <0.001) even after adjustment for lipid and lipoprotein concentrations. CONCLUSIONS: Women have a less atherogenic subclass profile than men, even after accounting for differences in lipid concentrations.     

低密度、氧化低密度脂蛋白对内皮细胞分泌内皮素的影响

目的 观察低密度脂蛋白（LDL）、氧化低密度脂蛋白（ox-LDL）对内皮细胞分泌内皮素（ET）的影响，以及后者在体外是否对前者具有氧化修饰作用.方法 采用不同浓度的LDL、ox-LDL及LDL＋ox-LDL与脐静脉内皮细胞株ECV-304进行孵育，24 h后分别收集细胞和上清液，采用放免分析法测定ET含量.结果 LDL、ox-LDL均能促进内皮细胞合成、分泌ET，但ox-LDL的作用更显著，而LDL＋ox-LDL组上清ET浓度大于两者单独作用之和.结论 LDL、ox-LDL均能促进内皮细胞合成、分泌ET，但后者的作用更为明显，且在体外对LDL具有氧化修饰作用。