【作者】 丁月霞； 刘启才；

【Author】 DING Yue-xia~1 LILT Qi-cai~2(1.Department of Cardiology,the Second Affiliated hospital of Guangzhou Medical College,Guangdong 510260,China)

【机构】 广州医学院附属第二医院心内科； 广州医学院分子生物学中心；

【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 Western Blot 检测两种粘附分子的 mRNA 和蛋白表达水平;利用 Griees 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^-9 mol/L)即可刺激 HUVECs 表达 ICAM-1和 VCAM-1 mRNA,随浓度增加表达增强;10^-7 mol/L Ang Ⅱ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。更多还原

【Abstract】 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 apop- tosis,and lipoprotein peroxidation.Ang Ⅱalso 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 de- velopment of atherosclerotic lesions,AnglI may also be involved in acute complications of atherosclerosis by promoting plaque rapture and a hyperthrombotic 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^-7M 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）.Conclu- sions: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.更多还原