内皮微颗粒通过NADPH氧化酶损伤内皮细胞功能  

Role of NADPH oxidase in endothelial cell dysfunction induced by endothelial microparticles

作　　者：程飞[1] 陶军[1] 冯鉴强[2] 杨春涛[2] 王妍[1] 张媛媛[1] 张晓琳[1] 

机构地区：[1]中山大学附属第一医院高血压血管病科,广东广州510080 [2]中山大学中山医学院生理教研室,广东广州510080

出　　处：《南方医科大学学报》2010年第5期1103-1106,共4页Journal of Southern Medical University

摘　　要：目的探讨冠心病患者循环内皮微颗粒(EMPs)与血流介导的内皮舒张功能(FMD)之间的关系以及EMPs损伤内皮细胞功能的机制。方法选择2009年3～6月在中山大学附属第一医院高血压血管病科住院的冠心病患者及冠心病高危患者各15名,检测血生化指标、循环内皮微颗粒水平及血流介导的内皮舒张功能,分析各项指标之间的关系;培养人脐静脉内皮细胞(HUVECs),制备内皮细胞来源的微颗粒,用内皮微颗粒刺激培养的人脐静脉内皮细胞,检测活性氧产物(ROS)及一氧化氮(NO)的水平。结果冠心病患者硝酸酯类的使用比率高于冠心病高危患者,冠心病患者循环内皮微颗粒水平高于高危患者,而血流介导的内皮舒张功能低于高危患者,在所有患者中,循环内皮微颗粒水平与血流介导的内皮舒张功能之间呈负相关;EMPs呈浓度依赖性地增加脐静脉内皮细胞活性氧产物的产生,并降低NO的生成,应用20μmol/lNADPH氧化酶抑制剂Apocyine能显著抑制EMPs导致的ROS增加和NO的降低。结论在冠心病患者中,循环EMPs可以损伤内皮细胞舒张功能,NADPH氧化酶参与EMPs导致内皮细胞功能障碍的损伤过程。Objective To explore the correlation between circulating endothelial microparticles （EMPs） and flow-mediated dialation （FMD） in patients with coronary artery disease （CAD）, and investigate the role of NADPH oxidase in endothelial cell dysfunction caused by EMPs. Methods Fifteen patients with CAD and 15 at high risks of CAD were tested for the level of EMPs and FMD and other biochemical indices, and the correlation between the indices were analyzed. EMPs obtained from cultured human umbilical vein endothelial cells （HUVECs） were phenotyped and used to stimulate the HUVECs, whose ROS and NO production was tested. Results Endothelial dilation function could be damaged by circulating EMPs in CAD patients. Dysfunction of HUVECs caused by 105/ml EMPs could be reversed by pretreatment with 20 μmol/L apocynin, a NADPH oxidase inhibitor. Conclusion Endothelial dialation function of the endothelial cells can be damaged by circulating EMPs in patients with CAD in association with NADPH oxidase activation.

关 键 词：内皮微颗粒 NADPH氧化酶 活性氧产物 一氧化氮 内皮细胞功能障碍 

分 类 号：R541.4[医药卫生—心血管疾病]