Exploring Biological Mechanism and Potential Targets of "Heat-toxin Stagnation in Collaterals" in AECOPD Based on Neutrophil Extracellular Traps
10.13422/j.cnki.syfjx.20260895
- VernacularTitle:基于中性粒细胞胞外陷阱探析AECOPD“热毒滞络”生物学机制及其潜在靶点
- Author:
Yang CUI
1
;
Jiaran WANG
1
;
Lijian PANG
2
;
Linlin WANG
2
;
Xiaodong LYU
3
Author Information
1. College of Basic Medical Sciences，Liaoning University of Traditional Chinese Medicine （TCM）， Shenyang 110847，China
2. The Affiliated Hospital of Liaoning University of TCM，Shenyang 110032，China
3. Administration of Liaoning University of TCM，Shenyang 110847，China
- Publication Type:Journal Article
- Keywords:
acute exacerbation of chronic obstructive pulmonary disease （AECOPD）;
collateral disease;
neutrophil extracellular traps （NETs）;
heat-toxin stagnation in collaterals;
target
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(22):299-307
- CountryChina
- Language:Chinese
-
Abstract:
Acute exacerbation of chronic obstructive pulmonary disease （AECOPD） belongs to the pulmonary collateral disease of traditional Chinese medicine， and its pathogenesis is always lung deficiency and blood stasis， heat and toxin stagnation. Lung deficiency and blood stasis are the pathological basis of COPD， and heat and toxin stagnation lead to acute exacerbation of the disease. Currently， there are few direct studies on the intervention of traditional Chinese medicine regulating NETs in AECOPD， but based on the idea of treating similar diseases differently， exploring NETs as a biological target for "heat toxin blocking the meridians" can provide modern theoretical support for the traditional Chinese medicine treatment method of clearing heat and regulating meridians for AECOPD， and provide new ideas for the mechanism research and new drug development of AECOPD. Studies have shown that the overproduction of neutrophil extracellular traps （NETs） can mediate lung inflammation and damage lung epithelial and endothelial cells， which is intrinsically consistent with the pathogenesis of this traditional Chinese medicine. Based on the theory of collateral disease， this paper combs the relevant generation pathways of NETs and the modern scientific mechanism of NETs involved in the pathogenesis of AECOPD， analyzes the correlation between the pathogenesis of AECOPD "heat and toxin stagnation" and the biological effects of NETs， and summarizes the potential targets of traditional Chinese medicine to regulate nets in the prevention and treatment of AECOPD. NETs can damage the airway epithelium and alveolar microvascular endothelium through cytotoxic effects， activate multiple inflammatory signaling pathways to release a large number of pro-inflammatory factors， induce mucus hypersecretion and promote thrombosis， and mediate the occurrence and development of AECOPD. This pathological process corresponded to the pathogenesis of heat and poison burning the qi collaterals of the lung， consuming the blood collaterals， and brewing phlegm and blood stasis over time. Existing studies have shown that traditional Chinese medicine monomers， compounds and acupuncture and moxibustion can inhibit the Peptidylarginine deiminase 4（PAD4）， nicotinamide adenine dinucleotide phosphate（NADPH） oxidase 2（NOX2）， nuclear factor-κB（NF-κB）， Toll like protein（TLR） and other signaling pathways， reduce the excessive release of NETs， play a role in clearing heat and dredging collateral， detoxification and blood stasis， and reduce lung tissue damage. At present， there are few direct studies on the regulation of NETs by traditional Chinese medicine in AECOPD. However， relying on the idea of treating different diseases together， mining NETs as the biological target of "heat and toxin stagnation" can provide modern theoretical support for the treatment of AECOPD with traditional Chinese medicine to clear heat and clear collaterality， and provide new ideas for the mechanism research and new drug research and development of AECOPD.
