Cardamine flexuosa extract attenuates neutrophilic airway inflammation in a CSE/LPS-induced murine model

Introduction Chronic 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. Methods This 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. Results In 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. Conclusion These 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.