Qingjin Huatan decoction attenuates lipopolysaccharide-induced acute lung injury in mice by controlling platelet-associated formation of neutrophil extracellular traps
10.1097/st9.0000000000000006
- Author:
Shunli XIAO
1
;
Yilin WANG
1
;
Lu LIU
1
;
Zhengxiao SUN
1
;
Jing XU
1
;
Xiaojie YIN
1
;
Xin WANG
2
;
Fulong LIAO
1
;
Yun YOU
1
;
Huamin ZHANG
1
Author Information
1. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China
2. Molecular Cardiology Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK
- Publication Type:Journal Article
- Keywords:
Qingjin Huatan Decoction;
Acute lung injury;
Neutrophil extracellular traps;
Neutrophils;
Platelets;
Transcriptomics
- From:
Science of Traditional Chinese Medicine
2023;1(1):59-71
- CountryChina
- Language:English
-
Abstract:
Background: Acute lung injury (ALI) is a severe and life-threatening lung inflammation with high morbidity and mortality, underscoring the importance to develop effective drugs. Qingjin Huatan decoction (QJHTD), as a classic ancient prescription, has been widely used for treating respiratory diseases. However, the role and mechanism of QJHTD against ALI remain unclear. Objective: This study aimed to explore the therapeutic effect of QJHTD on lipopolysaccharide (LPS)-induced ALI in mice and uncover its mechanism. Methods: The therapeutic effect of QJHTD on LPS-induced ALI in mice was evaluated by the histopathological changes in the lung tissue, the lung wet/dry weight ratio, and the levels of inflammatory cytokines and thrombin-antithrombin complexes. Transcriptomics was used to predict the mechanism of QJHTD in treating ALI. The expression levels of citrullinated histone 3 in the lung tissue, the content of cell-free DNA in the bronchoalveolar lavage fluid (BALF), and the platelet-associated formation of neutrophil extracellular traps (NETs) in vitro were determined. Results: Qingjin Huatan decoction exerted protective effect against LPS-induced ALI by suppressing interstitial edema, maintaining the alveolar-capillary barrier, inhibiting the infiltration of neutrophils and platelets in the lung tissue, and lowering the levels of tumor necrosis factor α, interleukin 1β, interleukin 6, and thrombin-antithrombin complexes in BALF. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis indicated that the formation of NETs was the main regulatory pathway for QJHTD against ALI. Qingjin Huatan decoction could treat ALI by inhibiting the release of NETs via reducing the content of citrullinated histone 3 in lung tissue and cell-free DNA in BALF in vivo, and suppressing the NETs formation induced by LPS-stimulated platelets under flow and static conditions in vitro. The formation of NETs was considered to bridge the interactions between neutrophils and platelets. Conclusions: This research demonstrated the effects of QJHTD in treating ALI and provided new insights for clarifying the complex regulation of neutrophils, platelets, and NETs in ALI.
