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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 7042872, 11 pages
Research Article

The Inhibitory Effect of WenxinKeli on H9C2 Cardiomyocytes Hypertrophy Induced by Angiotensin II through Regulating Autophagy Activity

1Guang’anmen Hospital, Chinese Academy of Chinese Medical Sciences, Beijing 100053, China
2Key Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China
3Department of Cardiology, General Hospital of People’s Liberation Army, Beijing 100853, China
4Xuan Wu TCM Hospital, Beijing 100053, China
5Masonic Medical Research Laboratory, Utica, NY 13501, USA

Correspondence should be addressed to Hongcai Shang; moc.621@iacgnohgnahs and Yanwei Xing; moc.361@54321iewnaygnix

Received 13 March 2017; Accepted 2 May 2017; Published 20 June 2017

Academic Editor: Veronika A. Myasoedova

Copyright © 2017 Jie Li 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.


Objectives. We investigated the role of cardiomyocyte autophagy and its regulatory mechanisms by WenxinKeli (WXKL) in cells subjected to hypertrophy. Methods. H9C2 cardiomyocytes were divided into 8 groups. Cytoskeletal proteins as well as endogenously expressed autophagy marker proteins were studied by confocal imaging. Western blotting was used to assess the levels of light chain-3 (LC3) and mechanistic target of rapamycin (mTOR). The cell viability assay was used to detect the content of ATP. Flow cytometry was used to detect apoptotic cardiomyocytes. Results. (1) Compared with the control group, the length and width of cells in the Angiotensin II (AngII) group were significantly increased, while those in the 3-methyladenine (3-MA) and the WXKL groups were decreased. (2) Compared with AngII group, the expression of LC3 II/I protein in the 3-MA and WXKL groups was downregulated, while the expression of mTOR protein was upregulated. (3) Compared with the AngII group, the cardiomyocytes in the WXKL group showed increased ATP and decreased apoptosis rate and number of autophagosome. Conclusions. We propose a novel role of WXKL as a likely inhibitor of cardiac hypertrophy by regulation of pathological autophagy.