OBJECTIVETo study the protective effects of PPAR gamma ligand rosiglitazone (RGZ) against hyperoxia-induced lung injury in neonatal rats.

METHODSNinety-six neonatal Sprague-Dawley (SD) rats were randomly divided into three groups: control (room air exposure), hyperoxia (85%-90% oxygen exposure) and RGZ treatment [85%-90% oxygen exposure plus RGZ solution injection (2 mg/kg, once daily)］. Rats were sacrificed at 1, 3, 7 and 14 days after exposure. Hematoxylin and eosin staining was used to evaluate histological changes in lung tissues. The contents of malondialdehyde (MDA) and leucocyte count in bronchoalveolar lavage fluid (BALF) were measured.

RESULTSNo pathological changes were found in the control group at any time point after exposure. Alveolar epithelial cell swelling, interstitial edema and massive infiltration of inflammatory cells were found in the hyperoxia group 3 days after exposure. At 14 days after exposure, the number of pulmonary alveoli was reduced, alveolus interstitium had thickened and organizational structure had become disordered in the hyperoxia group. The RGZ treatment alleviated significantly the hyperoxia induced alterations in lung pathology. Radial alveoli count (RAC) decreased significantly in the hyperoxia group compared with the control group from 3 days through to 14 days after exposure (P<0.05). The RGZ treatment group showed significantly increased RAC compared with the hyperoxia group at 3, 7 and 14 days after exposure (P<0.05). MDA content and leucocyte count in BALF increased significantly in the hyperoxia group 3 days after exposure (P<0.05), reached a peak 7 days after exposure (P<0.01) and remained higher 14 days after exposure (P<0.05) compared with the control group. The RGZ treatment group significantly decreased MDA content and leucocyte count compared with the hyperoxia group (P<0.05).

CONCLUSIONSHyperoxia may cause acute and chronic pulmonary injuries in neonatal rats, characterized by acute inflammatory reactions and decreased alveolus in lungs. RGZ may have protective effects against hyperoxia induced lung injury.