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Evidence-Based Complementary and Alternative Medicine
Volume 2018, Article ID 6705871, 8 pages
Research Article

Xiaoqinglong Decoction Attenuates Chronic Obstructive Pulmonary Disease in Rats via Inhibition of Autophagy

1Department of Integrated Traditional Chinese and Western Medicine, West China Hospital of Sichuan University, Chengdu 610041, China
2Institute of Life Sciences, Chongqing Medical University, Chongqing 400016, China

Correspondence should be addressed to Huanan Wang; moc.361@nhgnawxh

Received 31 July 2017; Revised 7 December 2017; Accepted 2 January 2018; Published 31 January 2018

Academic Editor: Subash C. Gupta

Copyright © 2018 Huanan 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.


Effective treatment for chronic obstructive pulmonary disease (COPD) and knowledge of the underlying mechanism are urgently required. Xiaoqinglong decoction (XQL) is widely used to treat COPD in Traditional Chinese Medicine, but the mechanism remains unclear. In this study, we tested the hypothesis that XQL ameliorates COPD via inhibition of autophagy in lung tissue on a rat model. Rats were divided into five groups, namely, Control group, COPD group, COPD + XQL group, COPD + Rapamycin group, and COPD + XQL + Rapamycin group. Pathological changes on cellular and molecular levels, apoptosis reflected by TdT-mediated dUTP Nick-End Labeling (TUNEL) assay, and autophagy represented by LC3II/LC3I ratio and p62 level were investigated for each group. Compared with the Control group, COPD rats exhibited structural changes and activated inflammation in the lung tissue, together with enhanced apoptosis and elevated autophagy biomarkers. XQL treatment significantly ameliorated these changes, while rapamycin augmented them. These data altogether confirmed the involvement of autophagy in the pathogenesis of COPD and suggested that XQL attenuates COPD via inhibition of autophagy.