Journal of ethnopharmacology · 2025
Lifei Qingchang Granules alleviate airway inflammation in a mouse model of bronchiectasis by inhibiting neutrophil extracellular traps.
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Yuanlong Hu, Wanyan Li, Jiamin Zeng, Shangke Gao, Yingsi Du, Ran Lin, Zhu Liang, Shiting Dai, Min Huang, Zhiming Pan, Qifen Huang, Zhijuan Wu, Xinghua Song, Shouxie Huang, Zhenqiu Li, Dapeng Zhang, Wenju Lu, Zhimin Zhang
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Lifei Qingchang Granules (LFQC) is a traditional Chinese medicine formula used to treat acute exacerbations and prevent recurrence of bronchiectasis. Excessive neutrophil extracellular trap (NET) formation has been increasingly recognized as a key driver of airway inflammation and tissue injury in bronchiectasis. However, the mechanism by which LFQC modulates NET dynamics remains unclear.
AIM OF STUDY: To evaluate the therapeutic efficacy and mechanism of LFQC in bronchiectasis, focusing on NET regulation.
MATERIALS AND METHODS: A recurrent Pseudomonas aeruginosa-induced mouse model of bronchiectasis was established and treated with LFQC. Airway inflammation and dilation were assessed by micro-CT, histology, and ELISA. In vivo and in vitro assays examined NET formation and oxidative stress, while LC-MS, network pharmacology, and molecular docking were applied to identify active compounds and their potential targets.
RESULTS: LFQC significantly reduced bacterial burden, airway dilation, and inflammatory infiltration in bronchiectasis mice. Levels of IL-1β, IL-6, TNF-α, MPO, and NE in bronchoalveolar lavage fluid were decreased. LFQC suppressed pulmonary NET formation and reduced Cit-H3, MPO, and NE expression. In vitro, LFQC-containing serum inhibited LPS-induced NETosis and ROS production by down-regulating the NOX2-p47 phox complex. Molecular docking revealed strong binding between LFQC components and NOX2/p47 phox.
CONCLUSION: LFQC alleviates airway inflammation in bronchiectasis by inhibiting NET formation through the NOX2-p47 phox/ROS pathway, supporting its potential as a therapeutic agent for bronchiectasis.
AIM OF STUDY: To evaluate the therapeutic efficacy and mechanism of LFQC in bronchiectasis, focusing on NET regulation.
MATERIALS AND METHODS: A recurrent Pseudomonas aeruginosa-induced mouse model of bronchiectasis was established and treated with LFQC. Airway inflammation and dilation were assessed by micro-CT, histology, and ELISA. In vivo and in vitro assays examined NET formation and oxidative stress, while LC-MS, network pharmacology, and molecular docking were applied to identify active compounds and their potential targets.
RESULTS: LFQC significantly reduced bacterial burden, airway dilation, and inflammatory infiltration in bronchiectasis mice. Levels of IL-1β, IL-6, TNF-α, MPO, and NE in bronchoalveolar lavage fluid were decreased. LFQC suppressed pulmonary NET formation and reduced Cit-H3, MPO, and NE expression. In vitro, LFQC-containing serum inhibited LPS-induced NETosis and ROS production by down-regulating the NOX2-p47 phox complex. Molecular docking revealed strong binding between LFQC components and NOX2/p47 phox.
CONCLUSION: LFQC alleviates airway inflammation in bronchiectasis by inhibiting NET formation through the NOX2-p47 phox/ROS pathway, supporting its potential as a therapeutic agent for bronchiectasis.