AVE 0991 attenuates cardiac hypertrophy through reducing oxidative stress
AVE 0991 attenuates cardiac hypertrophy through reducing oxidative stress
复制标题
AVE 0991 通过减少氧化应激减轻心脏肥大
DOI：
10.1016/j.bbrc.2015.09.050
复制
发表时间：
2016-06-10
影响因子：
3.1
通讯作者：
Chen, Yili
中科院分区：
文献类型：
--
作者：
Ma, Yuedong;Huang, Huiling;Chen, Yili
AVE 0991是一种非肽类血管紧张素-（1-7）（Ang-（1 -7））类似物，被认为具有有益的心血管作用。然而，其机制尚未完全阐明。本研究旨在探讨AVE 0991对心肌肥厚的影响及其机制。对小鼠进行主动脉结扎以诱导心脏肥大，然后给予AVE 0991（20 mg/kg/天（-1））4周。结果表明，AVE 0991减轻了左心室肥大，改善了心脏功能，其特征在于左心室重量和左心室舒张末期直径降低，射血分数增加。此外，AVE 0991显着下调平均肌细胞直径和衰减肥大标志物的基因表达。此外，AVE 0991抑制NOX 2和NOX 4的表达，这意味着AVE 0991降低心肌肥厚小鼠的氧化应激。我们的数据表明，AVE 0991治疗可以减轻心肌肥厚，改善心脏功能，这可能是由于减少氧化应激。(C)2016由Elsevier Inc.出版
AVE 0991, the nonpeptide angiotensin-(1-7) (Ang-(1-7)) analog, is recognized as having beneficial cardiovascular effects. However, the mechanisms have not been fully elucidated. This study was designed to investigate the effects of AVE 0991 on cardiac hypertrophy and the mechanisms involved. Mice were underwent aortic banding to induce cardiac hypertrophy followed by the administration of AVE 0991 (20 mg kg-day (-1)) for 4 weeks. It was shown that AVE 0991 reduced left ventricular hypertrophy and improved heart function, characterized by decreases in left ventricular weight and left ventricular end diastolic diameter, and increases in ejection fraction. Moreover, AVE 0991 significantly down-regulated mean myocyte diameter and attenuate the gene expression of the hypertrophic markers. Furthermore, AVE 0991 inhibited the expression of NOX 2 and NOX 4, meaning that AVE 0991 reduced oxidative stress of cardiac hypertrophy mice. Our data showed that AVE 0991 treatment could attenuate cardiac hypertrophy and improve heart function, which may be due to reduce oxidative stress. (C) 2016 Published by Elsevier Inc.