miR‐16‐5p Attenuated Airway Inflammation and Pulmonary Fibrosis of Asthma Rats by Regulating the TGF‐β1/Smad3 Signaling

Bronchial asthma is a significant inflammatory disorder impacting the airways. While current therapeutic interventions manage these symptoms, they do not offer a cure for the condition. Emerging research indicates that specific microRNAs (miRNAs) are implicated in the pathogenesis of asthma and the associated airway remodeling. Notably, miR-16-5p has been identified as a regulator of TGF-β1-induced epithelial-mesenchymal transition (EMT) in bronchial epithelial cells. This study investigates the influence of miR-16-5p on pulmonary function, inflammation, and fibrosis in asthma, focusing on its interaction with the TGF-β1/Smad3 signaling pathway, using a rat model for experimental analysis. Male Sprague-Dawley rats were given ovalbumin (OVA) and aluminum hydroxide to create an asthma model. They were divided into six groups. miRNA treatments were delivered using PEG-liposomes before each asthma challenge for 8 weeks. Asthma rats had lower levels of miR-16-5p. Elevating miR-16-5p levels improved breathing, reduced inflammation, and prevented lung damage. miR-16-5p regulated the TGF-β1/Smad3 pathway by targeting Smad3, indicating its protective role against asthma. Increasing miR-16-5p levels can improve lung function, reduce inflammation, and prevent lung fibrosis in asthma rats by targeting Smad3 to block the TGF-β1/Smad3 pathway. This finding suggests that miR-16-5p has translational potential as a novel therapeutic target for asthma treatment, which could lead to more effective strategies for asthma management in the future.