Simvastatin Improves Epithelial Barrier Function by Enhancing Alveolar Repair in Experimental Asthma

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Introduction: Asthma is a chronic inflammatory airway disease characterized by epithelial barrier dysfunction and persistent immune activation. Statins exhibit pleiotropic anti-inflammatory and immunomodulatory properties, but their therapeutic potential in asthma remains incompletely understood. This study aimed to investigate the effects of simvastatin on airway inflammation and epithelial barrier integrity in a murine model of experimental asthma and in airway epithelial cell systems. Methods: A murine model of experimental asthma was used to evaluate the effects of simvastatin on airway inflammation, cytokine production, and epithelial barrier function. In vitro airway epithelial cell models were employed to assess epithelial wound healing, tight junction protein expression, and inflammatory signaling pathways. Results: Simvastatin significantly reduced airway inflammation and pro-inflammatory cytokine levels while improving epithelial barrier integrity in vivo. These effects were associated with increased expression of tight junction proteins and epithelial repair mediators. In vitro experiments confirmed that simvastatin enhanced epithelial wound healing and modulated key inflammatory signaling pathways. Discussion: The findings indicate that simvastatin exerts protective effects on airway epithelial structure and immune responses, suggesting a potential role in restoring barrier function and reducing airway inflammation. These results provide mechanistic insight into the non-lipid-lowering benefits of statins in airway disease. Conclusion: Collectively, our findings demonstrate that simvastatin promotes alveolar epithelial repair by reducing apoptosis, enhancing proliferation, and restoring tight junction integrity, thereby improving overall barrier function.

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