欢迎访问《中国临床药理学与治疗学》杂志官方网站,今天是

中国临床药理学与治疗学 ›› 2005, Vol. 10 ›› Issue (2): 180-183.

• 研究原著 • 上一篇    下一篇

血管紧张素-(1-7) 对血管紧张素II致人脐静脉内皮细胞损伤的保护作用研究

邹军, 王虹, 冯丹1   

  1. 武汉大学中南医院综合医疗科, 医学院老年病研究所, 1医学院生理系, 武汉430071, 湖北
  • 收稿日期:2004-12-15 修回日期:2005-01-25 出版日期:2005-02-06 发布日期:2020-11-18
  • 通讯作者: 王虹, 女, 主任医师, 主要从事高血压、冠心病研究。E-mail:hongwang9@yahoo.com.cn
  • 作者简介:邹军, 男, 硕士研究生, 主要从事冠心病研究。Tel:027-87331194 E-mail:zoujun961@163.com

Protective effect of angiotensin-(1-7) on human umbilical vein endothelial cells injury induced by angiotensin II in culture

ZOU Jun, WANG Hong, FENG Dan1   

  1. Department of Internal Medicine and Geriatrics of Zhongnan Hospital, Institute of Geriatrics of Medical College, 1Department of physiology of Medical College, Wuhan University, Wuhan 430071, Hubei, China
  • Received:2004-12-15 Revised:2005-01-25 Online:2005-02-06 Published:2020-11-18

摘要: 目的:观察血管紧张素-(1-7) [Ang-(1-7)] 对血管紧张素II(Ang II) 致人脐静脉内皮细胞(HUVECs)损伤的保护作用。方法:体外培养的HUVECs随机分为4 组:对照组, AngII 组, Ang-(1-7) 组, AngII+Ang-(1-7) 组。采用分光光度计测定培养的HUVECs乳酸脱氢酶(LDH) 漏出;流式细胞仪检测细胞凋亡;硝酸还原酶法和放射免疫分析技术分别测定HUVECs 上清液中一氧化氮(NO) 和内皮素-1(ET-1)的含量。结果:与对照组比较,Ang II(0.1 μmol°L-1)显著增加HUVECs LDH 漏出(P<0.01)、ET-1 分泌(P<0.01) 和HUVECs 凋亡率(P<0.01), 显著减少NO 的含量(P<0.05);Ang-(1-7) 呈剂量依赖性抑制了Ang II 的促LDH 漏出、ET-1 分泌、增加细胞凋亡等作用, 同时明显促进HUVECs 的NO 释放;单用Ang-(1-7) 对HUVECs 无明显影响。结论:Ang-(1-7)可抑制Ang II 所致的体外培养HUVECs 损伤, 对内皮细胞具有保护作用。

关键词: 血管紧张素-(1-7), 血管紧张素II, 人脐静脉内皮细胞, 凋亡, 一氧化氮, 乳酸脱氢酶, 内皮素

Abstract: AIM: To investigate the protective effects of angiotensin-(1-7) [Ang-(1-7)] on human umbilical vein endothelial cells (HUVECs) injury induced by angiotensin II (Ang II) in culture.METHODS: Cultured human umbilical vein endothelial cells were randomly divided into 4 groups:control, Ang II, Ang-(1-7), and AngII+Ang-(1-7).Spectrophotometer and flow cytometry were used to evaluate lactate dehydrogenase (LDH) leakage content and apoptosis percentage, respectively. Nitric oxide (NO) and endothelin-1 (ET-1) contents were measured by colorimetry and radioimmunoassay.RESULTS: 0.1 μmol°L-1 Ang II significantly increased LDH leakage (P<0.01), ET-1 release (P<0.01), and apoptosis percentage (P<0.01).These increases were inhibited by Ang-(1-7) in a dose-dependent manner, while NO release by HUVECs was promoted by Ang-(1-7).Ang-(1-7) alone had no effect on HUVECs. CONCLUSION: Ang-(1-7) has a protective effect on HUVECs via inhibition of Ang II-induced injury and apoptosis, suggesting that Ang-(1-7) may play an important role in prevention and treatment of vascular diseases.

Key words: angiotensin-(1-7), angiotensin II, human umbilical vein endothelial cells, apoptosis, nitric oxide, lactate dehydrogenase, endothelin

中图分类号: