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|本期目录/Table of Contents|

替米沙坦对压力负荷过重所致心衰大鼠心肌ACE2和AT1R表达的影响

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2016年第1期
页码:
29-032
栏目:
基础研究
出版日期:
2015-09-15

文章信息/Info

Title:
Effect of telmisartan on ACE2 expression in rat hearts with pressure overload-induced heart failure
作者:
韩振华1李永勤1王世捷2范艳梅1王 蓉1王聪霞1林元喜2
(西安交通大学:1.第二附属医院心内科;
2.医学部生理学与病理生理学系,陕西 西安 710004)
Author(s):
HAN Zhen-hua1 LI Yong-qin1 WANG Shi-jie2 FAN Yan-mei1 WANG Rong1 WANG Cong-xia1 LIN Yuan-xi2
(1.Department of Cardiology, Second Affiliated Hospital, 2.Department of Physiology and Pathophysiology, Health Science Center, Xi'an Jiaotong University, Xi’an 710004, Shaanxi, China)
关键词:
心力衰竭替米沙坦血管紧张素转化酶2MAS 血管紧张素Ⅱ血管紧张素Ⅱ1型受体
Keywords:
heart failure telmisartan ACE2 MAS AngII AT1R
分类号:
R453
DOI:
-
文献标识码:
A
摘要:
目的 探讨替米沙坦对压力负荷过重所致心衰大鼠血管紧张素Ⅱ(AngⅡ)、心肌血管紧张素Ⅱ1型受体(AT1R)、血管紧张素转化酶2(ACE2)及MAS蛋白表达的影响。方法 采用SD雄性大鼠通过腹主动脉缩窄术构建压力负荷性心肌肥厚致心力衰竭(HF)模型。将大鼠随机分为假手术对照组(n=12)、HF模型组(n=12)和替米沙坦干预组(n=12)。替米沙坦干预组每天给予替米沙坦连续8周,检测各组大鼠血流动力学参数、心脏指数、血浆AngⅡ含量、心肌中AT1R、ACE2和MAS蛋白的表达情况。结果 HF模型组心脏指数、血流动力学指标、血浆AngⅡ的含量及心肌AT1R、ACE2蛋白的表达明显升高(P<0.01),MAS蛋白表达明显下降(P<0.01);替米沙坦干预组心脏指数、血流动力学指标明显下降(P<0.01),血浆AngⅡ的含量及心肌AT1R蛋白的表达明显下降(P<0.01),而MAS和ACE2蛋白的表达明显升高(P<0.01)。结论 应用替米沙坦可明显改善HF大鼠心室重构,可能与AngⅡ和AT1R的下调,而MAS和ACE2的上调有关。
Abstract:
AIM To study the effect of telmisartan on AngII level, AT1R, ACE2 and MAS protein expressions in overload-induced heart failure of rats. METHODSMale Sprague Dawley rats (weighing 250 g) were used to construct the pressure overload-induced heart failure model through aortic stenosis surgery. Animals were randomly divided into three groups: sham control group (n=12), heart failure model group (HF, n=12) and telmisartan intervention group (n=12). Hemodynamics, heart MASs index and left ventricular MASs index, circulating and cardiac levels of angiotensin II, ACE2, AT1R and MAS protein expressions were evaluated at week 8. RESULTSThe hemodynamic meters, HMI and LVMI in HF group, improved significantly compared with those in sham control group (P<0.01). Levels of AngII, AT1R and ACE2 protein increased significantly in HF group (P<0.01), whereas MAS protein expressions decreased significantly compared with those in sham control group (P<0.01). The hemodynamic meters, HMI and LVMI in telmisartan group, were significantly lower than those in HF group (P<0.01). Levels of AngII and AT1R protein expressions were significantly lower in telmisartan group (P<0.01), whereas MAS and ACE2 protein expressions were significantly higher compared with those in the HF group (P<0.01). CONCLUSIONBoth downregulation of AngII-ACE-AT1 axis and upregulation of Ang (1-7)-ACE2-MAS axis may be involved in reversal of myocardial remodeling in heart failure by telmisartan.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期:2015-03-12.
>基金项目:西安交通大学科研项目资助(xjj2012148);陕西省自然科学基础研究项目资助(2013JQ4002)
通讯作者:王世捷,副教授,主要从事心血管疾病发病机制研究 Email:wshjem@163.com
作者简介:韩振华,副主任医师,博士 Email:drhanzhenhua@163.com
更新日期/Last Update: 2015-09-16