Caveolae在剪切应激诱导的内皮型一氧化氮合酶活化中的作用  

The Role of Caveolae in Shear Stress-induced Endothelial Nitric-oxide Synthase Activation

作　　者：李银萍[1] 欧阳静萍[1] 郑汉巧[1] 余追[2] 王保华[1] 

机构地区：[1]武汉大学医学院病理与病理生理学系,武汉430071 [2]武汉大学中南医院急诊科,武汉430071

出　　处：《生物医学工程学杂志》2005年第5期1020-1023,共4页Journal of Biomedical Engineering

基　　金：国家自然科学基金资助课题(30270531)

摘　　要：探讨不同水平剪切应激对内皮细胞型一氧化氮合酶(Endothelial nitric-oxide synthase,eNOS)活化的影响及Caveolae在其中的作用。通过硝酸还原法测定细胞灌流液中的一氧化氮(NO)水平,检测不同水平剪切应激对培养人脐静脉内皮细胞(HUVEC)NO合成水平及胆固醇结合剂Filipin(10μg/ml)作用对剪切应激诱导细胞eNOS活化的影响。同时用透射电镜观察细胞内Caveolae的形态。实验发现随着剪切应激水平的升高,内皮细胞中NO的合成增高;Filipin作用细胞后,剪切应激诱导的NO合成显著降低,而去除Filipin后,同一水平剪切应激诱导的细胞NO合成部分恢复。因此,剪切应激能诱导eNOS活化,且Caveolae在其中起关键作用。This article deals with the influence of shear stress on endothelial NO synthesis, and the role of caveolae in shear stress-induced eNOS activation. Human umbilical vascular endothelial cells （HUVEC） were cultured and exposed to different levels of laminal shear stress and Filipin, the perfused cultures were collected, and NO^2-/NO^3- was detected using nitrate reduction method. The structure of caveolae was observed through transmission electron microscopy （TEM ）. The level of NO^2-/NO^3- was found to increase with the elevation of shear stress level（P〈0. 01）. It was the highest at 1. 5 N/m^2. After treatment with Filipin, the level of NO produced by HUVEC decreased significantly（P〈0.01）, but after recovery and shear without Filipin, the level of NO synthesis bounded back （P 〈 0. 01）. It was then concluded that shear stress can induce endothelial NO synthesis and caveolae plays a key role in shear stress-induced eNOS activation.

关 键 词：剪切应激 小窝 小窝蛋白 内皮型一氧化氮合酶(eNOS) 一氧化氮(NO) 内皮细胞型一氧化氮合酶 CAVEOLAE 应激诱导 酶活化 剪切 内皮型 人脐静脉内皮细胞 应激水平 NO合成 

分 类 号：R363[医药卫生—病理学]