Cardamine flexuosa extract attenuates neutrophilic airway inflammation in a CSE/LPS-induced murine model
Abstract
IntroductionChronic obstructive pulmonary disease (COPD) is a leading cause of disease- related mortality worldwide and is characterized by progressive airflow limitation accompanied by persistent neutrophilic airway inflammation. Macrophage activation plays a key role in this process through the production of pro- inflammatory mediators and neutrophil-attracting chemokines.MethodsThis study investigated the anti-inflammatory effects of Cardamine flexuosa extract (CFE) in macrophage and cigarette smoke extract (CSE)/lipopolysaccharide (LPS)- induced models, with emphasis on macrophage inflammatory responses and neutrophilic airway inflammation.ResultsIn LPS-stimulated RAW 264.7 macrophages, CFE reduced nitric oxide production by 77.8% and decreased the secretion of TNF-α, IL-1β, IL-6, and matrix metalloproteinases (MMPs), accompanied by reduced MAPK phosphorylation. In a murine model induced by intranasal administration of CSE and LPS, oral CFE reduced total inflammatory cell and neutrophil counts in bronchoalveolar lavage fluid (BALF) by 53.9% and 82.9%, respectively, at 200 mg/kg compared with the CSE/LPS group. These effects were associated with reduced pulmonary expression of CXCL-1 and MIP-2 and decreased MAPK phosphorylation. Histological analysis demonstrated attenuation of inflammatory cell infiltration and mucus hypersecretion.ConclusionThese findings demonstrate that CFE attenuates macrophage inflammatory responses and neutrophilic airway inflammation in the CSE/LPS-induced murine model, accompanied by reduced inflammatory mediator production and MAPK activation.
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BibTeX
@article{kim2026cardamine,
title = {{Cardamine flexuosa extract attenuates neutrophilic airway inflammation in a CSE/LPS-induced murine model}},
author = {So Yeon Kim and Yoo Kyong Han and Dong-Seon Kim and Won-Kyung Yang and Seung-Hyung Kim and Eunjung Son and Yoon-Young Sung},
journal = {Frontiers in Pharmacology},
year = {2026},
month = nov,
doi = {10.3389/fphar.2026.1897816},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1897816},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Cardamine flexuosa extract attenuates neutrophilic airway inflammation in a CSE/LPS-induced murine model
AU - So Yeon Kim
AU - Yoo Kyong Han
AU - Dong-Seon Kim
AU - Won-Kyung Yang
AU - Seung-Hyung Kim
AU - Eunjung Son
AU - Yoon-Young Sung
PY - 2026
DA - 2026/11/02
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1897816
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.1897816
AB - IntroductionChronic obstructive pulmonary disease (COPD) is a leading cause of disease- related mortality worldwide and is characterized by progressive airflow limitation accompanied by persistent neutrophilic airway inflammation. Macrophage activation plays a key role in this process through the production of pro- inflammatory mediators and neutrophil-attracting chemokines.MethodsThis study investigated the anti-inflammatory effects of Cardamine flexuosa extract (CFE) in macrophage and cigarette smoke extract (CSE)/lipopolysaccharide (LPS)- induced models, with emphasis on macrophage inflammatory responses and neutrophilic airway inflammation.ResultsIn LPS-stimulated RAW 264.7 macrophages, CFE reduced nitric oxide production by 77.8% and decreased the secretion of TNF-α, IL-1β, IL-6, and matrix metalloproteinases (MMPs), accompanied by reduced MAPK phosphorylation. In a murine model induced by intranasal administration of CSE and LPS, oral CFE reduced total inflammatory cell and neutrophil counts in bronchoalveolar lavage fluid (BALF) by 53.9% and 82.9%, respectively, at 200 mg/kg compared with the CSE/LPS group. These effects were associated with reduced pulmonary expression of CXCL-1 and MIP-2 and decreased MAPK phosphorylation. Histological analysis demonstrated attenuation of inflammatory cell infiltration and mucus hypersecretion.ConclusionThese findings demonstrate that CFE attenuates macrophage inflammatory responses and neutrophilic airway inflammation in the CSE/LPS-induced murine model, accompanied by reduced inflammatory mediator production and MAPK activation.
SN - 1663-9812
ER -