cardioprotective effects of qishenyiqi mediated by angiotensin ii type 1 receptor blockade and enhancing angiotensin-converting enzyme 2心血管效应qishenyiqi介导的血管紧张素ⅱ1型受体封锁和增强血管紧张素转换酶2.pdfVIP

Hindawi Publishing Corporation Evidence-Based Complementary and Alternative Medicine Volume 2012, Article ID 978127, 9 pages doi:10.1155/2012/978127 Research Article Cardioprotective Effects of Qishenyiqi Mediated by Angiotensin II Type 1 Receptor Blockade and Enhancing Angiotensin-Converting Enzyme 2 Yong Wang,1 Chun Li,1 Yulin Ouyang,1 Junda Yu,1 Shuzhen Guo,1 Zhongyang Liu,2 Dong Li,2 Jing Han,1 and Wei Wang1 1 Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, Chao Yang District, Beijing 100029, China 2 State Key Laboratory of Proteomics, Beijing Proteome Research Center, Institute of Radiation Medicine, Beijing 100850, China Correspondence should be addressed to Wei Wang, wangwei 8@ Received 24 July 2012; Revised 15 October 2012; Accepted 22 October 2012 Academic Editor: Ching Liang Hsieh Copyright © 2012 Yong Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The aim of this paper was to investigate whether the effects of QSYQ on CHD are associated with the renin-angiotensin-aldosterone system (RAAS). The formula groups were lavaged with QSYQ, using fosinopril sodium as a control. The level of RAAS components in the myocardial tissue was measured, respectively. The results showed that both QSYQ and fosinopril sodium can improve the ejection fraction in CHD and that QSYQ decreases the left ventricular end-systolic diameter and left ventricular end-diastolic diameter, while fosinopril sodium has no effects on these parameters. Fosinopril sodium, as an ACE inhibitor, downregulated ACE expression and eventually reduced the tissue AngII concentration but had no effect on ACE2. Moreover, it had no