| 注册
首页|期刊导航|中国现代医学杂志|线粒体介导产生的活性氧在血管紧张素Ⅱ诱导的肾脏损害中的作用*

线粒体介导产生的活性氧在血管紧张素Ⅱ诱导的肾脏损害中的作用*

冯苗苗 刘素晓 王小晓 崔琳 谢世阳 沈思 朱明军 王幼平

中国现代医学杂志2017,Vol.27Issue(2):13-18,6.
中国现代医学杂志2017,Vol.27Issue(2):13-18,6.DOI:10.3969/j.issn.1005-8982.2017.02.002

线粒体介导产生的活性氧在血管紧张素Ⅱ诱导的肾脏损害中的作用*

Role of mitochondrial reactive oxygen species in angiotensinII-induced renal injury

冯苗苗 1刘素晓 2王小晓 2崔琳 2谢世阳 2沈思 2朱明军 2王幼平2

作者信息

  • 1. 河南中医学院 中西医结合临床学科,河南 郑州 450008
  • 2. 河南中医学院第一附属医院,河南 郑州 450000
  • 折叠

摘要

Abstract

Objective To clarify the role of mitochondrial reactive oxygen species (ROS) in angiotensin II (AngII)-induced renal injury by use of a specific scavenger of mitochondrial ROS, mitoTEMPO. Methods The mouse model of Ang II-dependent hypertension was induced with infusion of Ang II via subcutaneous miniosmotic pump, and the sham mice were given with normal saline. The Ang II-dependent hypertensive mice were divided into control (Ang II) group and experimental (Ang II + mitoTEMPO) group, which were subcutaneously administered with solvent and mitoTEMPO, respectively. Tail-cuff systolic blood pressure, and urinary excretion of 8-isoprostane and albumin, creatinine clearance, and the levels of mitochondrial ROS in the kidneys were assayed, and pathological changes of renal tissues were analyzed after 4 weeks of treatment. Results Compared with the sham mice, Ang II infusion led to increased systolic blood pressure and urinary excretion of 8-isoprostane and albumin, decreased creatinine clearance, and enhanced glomerulosclerosis index and renal tubulointerstitial injury ( < 0.05). The results were accompanied by the enhanced mitochondrial ROS production in the kidneys ( < 0.05). However, the treatment with mitoTEMPO alleviated all the above changes except for blood pressure, leading to renal protection ( <0.05). Conclusions Treatment with a specific scavenger of mitochondrial ROS, mitoTEMPO, can inhibit renal injury during Ang II-dependent hypertension, which is associated with the decreased mitochondrial ROS production in the kidneys. Thus, the results suggest that mitochondrial ROS can promote Ang II-induced renal injury.

关键词

血管紧张素Ⅱ/高血压/肾脏损害/线粒体/活性氧

Key words

angiotensin II/hypertension/renal injury/mitochondria/reactive oxygen species

分类

医药卫生

引用本文复制引用

冯苗苗,刘素晓,王小晓,崔琳,谢世阳,沈思,朱明军,王幼平..线粒体介导产生的活性氧在血管紧张素Ⅱ诱导的肾脏损害中的作用*[J].中国现代医学杂志,2017,27(2):13-18,6.

基金项目

国家自然科学基金(No81170243);河南省科技创新杰出人才项目(No124200510007);河南省科技攻关计划项目 ()

中国现代医学杂志

OACSTPCD

1005-8982

访问量0
|
下载量0
段落导航相关论文