British journal of pharmacology · 2026
β3-adrenoceptor agonism exerts lung protection in a rat model of bronchopulmonary dysplasia.
СтатьяНазвание и аннотация: Перевод в очереди
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Pini Alessandro, Nardini Patrizia, Zizi Virginia, Molino Marta, Calvani Maura, Carrozzo Francesco, Amato Rachele, Guasti Daniele, Biagini Denise, di Francesco Fabio, Silvestri Ludovico, Franceschini Alessandra, Bani Daniele, Imbimbo Elisa, Filippi Luca
Аннотация
BACKGROUND AND PURPOSE: Bronchopulmonary dysplasia (BPD) affects premature newborns, particularly those receiving supplemental oxygen therapy. Exposure of underdeveloped lungs to oxygen levels higher than the intrauterine environment causes oxidative stress, impairing alveolarisation, vascularisation and causing fibrosis. The β3-adrenoceptor could represent a promising target for BPD treatment because of its oxygen-dependent regulation, ability to reduce oxidative stress and protection against intestinal hyperoxia-induced damage.
EXPERIMENTAL APPROACH: In this study, neonatal rat pups were reared under hyperoxia for 2 weeks to induce a BPD-like disease and treated with the β3-adrenoceptor agonist BRL37344 (1, 3 or 6 mg kg-1).
KEY RESULTS: Through oxidative stress, hyperoxia decreases pulmonary volume, impairs alveolarisation and vascularisation, and causes fibrosis and type II pneumocyte hyperplasia, thereby reducing survival rates. BRL37344 at 3 mg kg-1 counteracted these alterations, doubling survival rates.
CONCLUSIONS AND IMPLICATIONS: Our findings demonstrate a new role for β3-adrenoceptors in protecting the lungs from hyperoxic injury, suggesting its pharmacological activation as a strategy for treating Bronchopulmonary dysplasia of prematurity and, possibly, other lung fibrosis-related disorders.
EXPERIMENTAL APPROACH: In this study, neonatal rat pups were reared under hyperoxia for 2 weeks to induce a BPD-like disease and treated with the β3-adrenoceptor agonist BRL37344 (1, 3 or 6 mg kg-1).
KEY RESULTS: Through oxidative stress, hyperoxia decreases pulmonary volume, impairs alveolarisation and vascularisation, and causes fibrosis and type II pneumocyte hyperplasia, thereby reducing survival rates. BRL37344 at 3 mg kg-1 counteracted these alterations, doubling survival rates.
CONCLUSIONS AND IMPLICATIONS: Our findings demonstrate a new role for β3-adrenoceptors in protecting the lungs from hyperoxic injury, suggesting its pharmacological activation as a strategy for treating Bronchopulmonary dysplasia of prematurity and, possibly, other lung fibrosis-related disorders.