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Evidence-Based Complementary and Alternative Medicine
Volume 2018, Article ID 2373609, 11 pages
https://doi.org/10.1155/2018/2373609
Research Article

Qi-Dong-Huo-Xue-Yin Inhibits Inflammation in Acute Lung Injury in Mice via Toll-Like Receptor 4/Caveolin-1 Signaling

1Department of Emergency, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China
2Department of Respiratory Medicine, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China
3Department of Laboratory Medicine, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China
4Animal Experimental Center, Zhejiang Chinese Medical University, Hangzhou, China
5Accident and Emergency Department, Royal Free London NHS Foundation Trust, London, UK

Correspondence should be addressed to Li-Ying Xu; nc.ude.umcz@6121ylux and Wan-Ru Cai; moc.nuyila@urnawiac

Received 6 November 2017; Accepted 14 January 2018; Published 11 February 2018

Academic Editor: Caigan Du

Copyright © 2018 Li-Ying Xu 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

Acute lung injury (ALI) is a critical illness with no current effective treatment. Caveolin-1 indirectly activates inflammation-associated signaling pathways by inhibiting endothelial nitric oxide synthase (eNOS). This induces an imbalance between pro- and anti-inflammatory cytokine levels, which are involved in the pathogenesis of ALI. The compound Chinese prescription Qi-Dong-Huo-Xue-Yin (QDHXY) is efficacious for ALI treatment via an anti-inflammatory effect; however, the exact underlying mechanism is unknown. Therefore, we explored the protective effect of QDHXY against lipopolysaccharide- (LPS-) induced ALI in mice. Histopathological changes in mouse lung tissues were studied. Furthermore, alterations in the serum levels of pro- and anti-inflammatory cytokines were investigated. The levels of tumor necrosis factor- (TNF-)α, interleukin- (IL-) 6, IL-1β, and interferon-γ-induced protein 10 in bronchoalveolar lavage fluid were measured. Additionally, the expression levels of myeloid differentiation factor 88 (MyD88), caveolin-1, and eNOS were assessed. QDHXY significantly reduced lung infiltration with inflammatory cells and the production of serum pro- and anti-inflammatory cytokines and inhibited the expression of TNF-α, IL-1β, caveolin-1, and MyD88 but not eNOS. These indicate that QDHXY significantly improved the balance between pro- and anti-inflammatory cytokine levels, possibly by inhibiting the caveolin-1 signaling pathway. Therefore, QDHXY may be a potential treatment for ALI.