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Therapeutic effects of Lianhua Qingke on COPD and influenza virus-induced exacerbation of COPD are associated with the inhibition of NF-κB signaling and NLRP3 inflammasome responses. | LitMetric

Therapeutic effects of Lianhua Qingke on COPD and influenza virus-induced exacerbation of COPD are associated with the inhibition of NF-κB signaling and NLRP3 inflammasome responses.

Int Immunopharmacol

State Key Laboratory for Innovation and Transformation of Luobing Theory, Shijiazhuang Hebei 050035, China; Hebei Academy of Integrated Traditional Chinese and Western Medicine, Hebei 050035, China. Electronic address:

Published: December 2024

AI Article Synopsis

  • Lianhua Qingke (LHQK) is a traditional Chinese medicine that shows promise in treating respiratory diseases, particularly by reducing inflammation and improving airway health.
  • The study used mouse models to test LHQK's effectiveness against chronic obstructive pulmonary disease (COPD) and acute exacerbations caused by virus infections.
  • Results indicated that LHQK significantly enhanced lung function, reduced inflammation, and inhibited viral replication, while also affecting key signaling pathways in the body, indicating its potential as a treatment for COPD and related conditions.

Article Abstract

Lianhua Qingke (LHQK), a traditional Chinese medicine (TCM) used clinically for the treatment of respiratory diseases with acute tracheobronchitis, and cough, has demonstrated promising efficacy in suppressing inflammation, inhibitingmucin secretion, reducing goblet cell hyperplasia andmaintainingairway epithelial integrity. However, its efficacy in managing chronic obstructive pulmonary disease (COPD) progression, particularly virus-induced acute exacerbations of COPD (AECOPD),remains unclear. Here, cigarette smoke (CS)-induced COPD and CS+virus (influenza H1N1)-triggered AECOPD mouse models were employed to evaluated the therapeutic potential of LHQK. The findings demonstrated that LHQK treatment led to significant improved pulmonary function, suppressed pulmonary inflammation, alleviated lung histopathological changes, and preserved airway epithelial integrity in COPD mice. Additionally, LHQK treatment effectively inhibited viral replication in the lungs of AECOPD mice and decreased recruitment of immune cells (M1 macrophages, progenitor-exhausted T cells and CD8 + T cells) to the lungs. Western blot analysis indicated that the therapeutic effects of LHQK are associated with the inhibition ofNF-κB signaling and NLRP3 inflammasome activation. Collectively, these findings elucidate the underlying mechanisms by which LHQK mitigates COPD and AECOPD, thereby supporting its potential as a therapeutic option for individuals afflicted with these conditions.

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Source
http://dx.doi.org/10.1016/j.intimp.2024.113213DOI Listing

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