Apelin‐13 Protects Against Airway Inflammation, Oxidative Stress, and Epithelial–Mesenchymal Transition in a Chronic Asthma Model

ABSTRACT

Airway inflammation, epithelial–mesenchymal transition (EMT), and airway remodeling are critical pathophysiological characteristics of chronic asthma. Apelin‐13 (AP‐13), a significant isoform of the apelin peptide, exhibits a wide range of physiological functions. This study aimed to investigate the potential effects and regulatory mechanisms of AP‐13 in asthma. An ovalbumin (OVA)‐induced murine asthma model was established to evaluate oxidative stress biomarkers, inflammatory cell infiltration (eosinophils, neutrophils, and lymphocytes), and Th2 cytokine production (IL‐4, IL‐5, IL‐13) using enzyme‐linked immunosorbent assay (ELISA). Lung histopathology was assessed by hematoxylin and eosin (H&E) staining, while epithelial–mesenchymal transition (EMT) markers were quantified through reverse transcription quantitative polymerase chain reaction (RT‐qPCR), western blot analysis, and immunohistochemistry. Our results demonstrated that AP‐13 could alleviate oxidative stress, decrease the number of inflammatory cells, inhibit the release of Th2 cytokines, improve pathological changes, and suppress EMT in asthmatic mice. Collectively, our data suggest that AP‐13 could be a promising therapeutic agent for the treatment of asthma.