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Evidence-Based Complementary and Alternative Medicine
Volume 2015, Article ID 298631, 10 pages
Research Article

Beneficial Effects of Qili Qiangxin Capsule on Lung Structural Remodeling in Ischemic Heart Failure via TGF-1/Smad3 Pathway

1Department of Cardiology, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China
2Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing 100029, China
3The Key Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China

Received 25 May 2015; Revised 21 September 2015; Accepted 27 September 2015

Academic Editor: Se Eun Byeon

Copyright © 2015 Yaoyao He 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.


Qili qiangxin (QL) capsule is a traditional Chinese medicine that is widely used for the treatment of patients with chronic heart failure (CHF) of all etiologies, although the exact mechanisms of action remain unclear. CHF leads to pulmonary vascular remodelling and thickening of the alveolar-capillary barrier that may be important mechanisms in the poor clinical outcome in patients with end-stage heart failure. We examined whether QL could improve lung injury in ischemic CHF by reducing lung remodeling. Rats with myocardial infarct received QL (1.0 g/kg/day) for 4 weeks. Echocardiographic and morphometric measurements were obtained followed by echocardiography, histological staining, and immunohistochemical analysis of lung sections. CHF caused significant lung structural remodeling evidenced by collagen deposition and thickening of the alveolar septa after myocardial infarct that were greatly improved by QL. Lung weight increased after infarct with no evidence of pulmonary edema and was normalized by QL. QL also reduced lung transforming growth factor-β1 (TGF-β1), p-Smad3, tumor necrosis factor-α (TNF-α), and Toll-like receptor-4 (TLR4) expression. Thus, QL reduces lung remodeling associated with CHF, mainly by suppressing the TGF-β1/Smad3 signaling pathway. The mechanism may also involve inhibition of TLR4 intracellular signaling.