AngⅡ对血管内皮细胞表达粘附分子和释放NO的影响  

AngⅡ Stimulates Adhesion Molecules and reduces the production of NO in HUVECs

作　　者：丁月霞[1] 刘启才[2] 

机构地区：[1]广州医学院附属第二医院心内科,广东广州510260 [2]广州医学院分子生物学中心

出　　处：《中国民康医学》2007年第3期81-84,87,共5页Medical Journal of Chinese People’s Health

基　　金：广东省自然科学基金课题(04009589)

摘　　要：目的:观察AngⅡ对体外培养的人脐静脉内皮细胞(HUVECs)表达粘附分子(ICAM-1和VCAM-1)及内皮NO生成的影响,讨论三者之间的关系和可能机制。方法:采用胰蛋白酶消化法进行HUVECs的原代培养,3-5代用于实验;通过RT-PCR和W estern B lot检测两种粘附分子的mRNA和蛋白表达水平;利用G riees反应原理测定上清NO释放量。结果:HUVECs未活化时不表达VCAM-1而ICAM-1呈低表达状态;AngⅡ在生理浓度时(10-9mol/L)即可刺激HUVECs表达ICAM-1和VCAM-1 mRNA,随浓度增加表达增强;10-7mol/L AngⅡ在不同时间点刺激HUVECs 6 h即有ICAM-1 mRNA和VCAM-1 mRNA较高表达,但高峰有所不同,前者在10 h左右,后者为12 h。在AngⅡ刺激下两种粘附分子的蛋白表达水平和趋势与mRNA相似;并随浓度增加而明显抑制NO生成。结论:AngⅡ明显增强HUVECs表达粘附分子,并抑制其NO生成,具有显著的促炎和促动脉粥样硬化作用。Objective：Angiotensin Ⅱ （Ang Ⅱ ）, the effectors peptide of the renin -angiotensin system, has been implied in the pathogenesis of arteriosclerosis and hypertension on various levels. Ang Ⅱ - induced endothelial dysfunction, endothelial cell apoptosis, and lipoprotein peroxidation. Ang Ⅱ also induces cellular adhesion molecules and decreases NO, all of which participate in the induction of an inflammatory response in the vessel wall. In addition, while all of these effects contribute to neointima formation and development of atherosclerotic lesions, AngⅡ may also be involved in acute complications of atherosclerosis by promoting plaque rupture and a hyperthrombetic state. Accordingly, Ang Ⅱ appears to have a central role in the pathophysiology of arteriosclerosis. Methods： Human umbilical vein was isolated and culcured. Passage 3 -5 of cultured HUVECs were incubated for 2,6,9,12,24 h with 10^-7 M AngⅡ or 10^-9 - 10^-6M for 12 h. Results： Total RNA was extracted, and the expression of mRNA and protein of ICAM - 1 and VCAM - 1 was assessed by RT - PCR and Western Blot; While measured NO production via Griess （nitrate reductase method ）. Conclusions： Ang Ⅱ could stimulate the expressions of ICAM - 1 and VCAM - 1 on dose or time dependant beth RNA and protein. Another, Ang Ⅱ could decrease NO production on dose.

关 键 词：血管紧张素Ⅱ 细胞间粘附分子-1 一氧化氮 血管内皮细胞 表达 

分 类 号：R-33[医药卫生] R541.4