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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 378298, 9 pages
http://dx.doi.org/10.1155/2013/378298
Research Article

Protective Effect of Qiliqiangxin Capsule on Energy Metabolism and Myocardial Mitochondria in Pressure Overload Heart Failure Rats

1Integrative Medicine Department, Hebei Medical University, 361 Zhongshan Road, Shijiazhuang 050017, China
2Hebei Yiling Medical Research Institute, Shijiazhuang 050035, China
3Key Research Centre of State Administration of Traditional Chinese Medicine (Collateral Disease of Cardiovascular), Shijiazhuang 050035, China
4Key Laboratory of Collateral Disease of Hebei Province, Shijiazhuang 050035, China
5Yiling Hospital, Hebei Medical University, Shijiazhuang 050091, China

Received 17 November 2012; Revised 8 June 2013; Accepted 25 June 2013

Academic Editor: Keji Chen

Copyright © 2013 Junfang Zhang 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.

Abstract

Qiliqiangxin capsule (QL) was developed under the guidance of TCM theory of collateral disease and had been shown to be effective and safe for the treatment of heart failure. The present study explored the role of and mechanism by which the herbal compounds QL act on energy metabolism, in vivo, in pressure overload heart failure. SD rats received ascending aorta constriction (TAC) to establish a model of myocardial hypertrophy. The animals were treated orally for a period of six weeks. QL significantly inhibited cardiac hypertrophy due to ascending aortic constriction and improved hemodynamics. This effect was linked to the expression levels of the signaling factors in connection with upregulated energy and the regulation of glucose and lipid substrate metabolism and with a decrease in metabolic intermediate products and the protection of mitochondrial function. It is concluded that QL may regulate the glycolipid substrate metabolism by activating AMPK/PGC-1α axis and reduce the accumulation of free fatty acids and lactic acid, to protect cardiac myocytes and mitochondrial function.