Background
Bronchopulmonary dysplasia (BPD) is an important cause of respiratory illness in preterm newborns that
Conclusions
Tet demonstrated potent activity against hyperoxia-induced lung injury in newborn rats through NF-κB and ERK1/2 pathway inhibition.
Methods
A hyperoxia-induced lung injury model was established using newborn rats exposed to high O2 levels. The models were treated with various concentrations of Tet, and a lung function test was conducted. Then, the lung tissues and blood were collected to detect the effect of Tet on cell apoptosis, inflammatory response, and fibrosis. The effect of Tet on nuclear factor-kappa B (NF-κB) and extracellular signal-regulated kinase1/2 (ERK1/2) pathways was also determined.
Results
Lung function was decreased in hyperoxia-induced rats, and Tet could reverse this inhibiting effect. For oxidative stress, Tet caused an increase in the levels of antioxidant enzymes. The apoptosis rate and apoptosis-related proteins were decreased in hyperoxia-induced rats after Tet treatment. Additionally, Tet treatment could reduce inflammatory factor levels, while increasing CD4+IFN-γ+ T cell levels and decreasing CD4+IL-4+ T cell levels. Tet treatment was also able to inhibit the expression of fibrosis-related markers and NF-κB and ERK1/2 pathways. Conclusions: Tet demonstrated potent activity against hyperoxia-induced lung injury in newborn rats through NF-κB and ERK1/2 pathway inhibition.