Ciclesonide shows a lung-protective effect in neonatal hyperoxia-exposed rats

Bronchopulmonary dysplasia (BPD), a chronic lung disease primarily observed in premature infants, is attributed to a lung injury-repair imbalance. Studies of postnatal corticosteroids have failed to identify clear candidates to help alleviate high BPD rates without risks or adverse effects.

This study aimed to assess whether the systemic postnatal administration of an alternative glucocorticoid, ciclesonide, could attenuate alterations in lung structure and right ventricular hypertrophy in a hyperoxic rat BPD-like model.

In a hyperoxia-induced model of BPD-like lung injury, pups were maintained in oxygen-enriched atmosphere-hyperoxia or normoxia (room air) for 14 days after natural birth, and subcutaneous ciclesonide (0.5 mg/kg) was administered postnatally for 5 consecutive days. On postnatal day 14, lung function (peak inspiratory pressure and compliance), lung structure (radial alveolar count, mean linear intercept, and pulmonary vessel density), and right ventricular hypertrophy were assessed.

On day 14, the effects of hyperoxia exposure were more evident in untreated rats (impaired lung compliance and structure and right ventricular hypertrophy) than in normoxia-exposed animals. Ciclesonide administration was associated with smaller body weight changes and significantly improved lung compliance, alveolarization, lung vascular growth, and right ventricular hypertrophy.

Postnatal ciclesonide administration preserved lung function and structure and prevented right ventricular hypertrophy in a hyperoxic BPD-like model. These findings suggest that postnatal ciclesonide may be an alternative to existing corticosteroids for the treatment of BPD. However, long-term studies are required to validate these findings.