(135) found the activation of NLRP3 inflammasome in hyperoxia-induced BPD neonatal mice at 85% hyperoxia, resulting in increased IL-1β and abnormal alveolar formation, while the use of recombinant IL-1RA (blocking the interaction between IL-1 and its receptor) and glibenclamide (a compound that blocks the assembly of NLRP3 inflammasome) showed the effect of blocking inflammasomes and protecting lung structure compared with placebo-treated mice. This evidence concerns the gene NLRP3 and bronchopulmonary dysplasia.