3,4,5-Trihydroxycinnamic acid attenuates lipopolysaccharide (LPS)-induced acute lung injury via downregulating inflammatory molecules and upregulating HO-1/AMPK activation

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Title
3,4,5-Trihydroxycinnamic acid attenuates lipopolysaccharide (LPS)-induced acute lung injury via downregulating inflammatory molecules and upregulating HO-1/AMPK activation
Author(s)
Jae Won Lee; W Chun; Ok-Kyoung Kwon; Hyun Ah Park; Yourim Lim; Jae Hyeon Lee; Doo-Young KimJung Hee Kim; Hyeong Kyu Lee; Hyung Won RyuSei-Ryang OhKyung Seop Ahn
Bibliographic Citation
International Immunopharmacology, vol. 64, pp. 123-130
Publication Year
2018
Abstract
The increase in inflammatory cytokines and chemokines is a common denominator in the pathogenesis of acute lung injury (ALI) which are involved in the influx of inflammatory cells and lung damage. The aim of the present study was to evaluate the protective effect of 3,4,5-trihydroxycinnamic acid (THC) in lipopolysaccharide (LPS)-induced ALI. THC efficiently decreased the mRNA expression of interleukin-8 (IL-8) in LPS-stimulated A549 airway epithelial cells. THC induced heme oxygenase-1 (HO-1) expression in A549 cells. THC also increased the activation of AMP-activated protein kinase (AMPK) in A549 cells and RAW264.7 macrophages. In LPS-induced ALI in mice, THC significantly suppressed neutrophil influx and monocyte chemoattractant protein-1 (MCP-1) production in the bronchoalveolar lavage fluid (BALF). THC also attenuated the levels of neutrophil elastase (NE), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the BALF and serum. In addition, THC inhibited the expressions of inducible nitric oxide synthase (iNOS) and the activation of nuclear factor-kappa B (NF-κB) in the lung. These protective effects of THC were accompanied with HO-1 induction and AMPK activation. Taken together, the present study clearly demonstrates that THC significantly attenuates the LPS-induced ALI, suggesting that THC might be a valuable therapeutic adjuvant in airway inflammatory disorders.
Keyword
ALIAMPKAirway inflammationHO-1NeutrophilsTHC
ISSN
1567-5769
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.intimp.2018.08.015
Type
Article
Appears in Collections:
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
Ochang Branch Institute > Division of National Bio-Infrastructure > Bio-Resource Central Bank > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
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