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Effect of retinoic acid on oxygen‐induced lung injury in the newborn rat
Author(s) -
Ozer Esra Arun,
Kumral Abdullah,
Ozer Erdener,
Duman Nuray,
Yilmaz Osman,
Ozkal Sermin,
Ozkan Hasan
Publication year - 2005
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.20131
Subject(s) - bronchopulmonary dysplasia , medicine , lung , microvessel , fibrosis , pathology , pulmonary fibrosis , immunostaining , oxygen therapy , retinoic acid , gastroenterology , anesthesia , endocrinology , immunohistochemistry , gestational age , biology , pregnancy , biochemistry , genetics , gene
Oxygen‐induced lung injury is believed to lead to the development of bronchopulmonary dysplasia (BPD). To determine whether retinoic acid (RA) treatment prevents the development of BPD by minimizing lung injury, we investigated the effect of RA on the histopathologic characteristics of oxygen‐induced lung injury in a newborn rat model. Eighteen rat pups were divided into three groups: room air‐exposed control group (n = 5), oxygen‐exposed placebo group (n = 7), and RA‐treated oxygen‐exposed group (n = 6). Measurement of alveolar area, quantitation of secondary crest formation, microvessel count, evaluation of alveolar septal fibrosis, and smooth muscle actin (SMA) immunostaining were performed to assess oxygen‐induced changes in lung morphology. Treatment of oxygen‐exposed animals with RA resulted in a significant increase in mean alveolar area; however, it had no effect on the number of secondary crests and microvessel count. The degree of fibrosis and SMA expression showed a significant decrease in RA‐treated animals. We conclude that RA treatment improves alveolar structure and decreases fibrosis in the newborn rat with oxygen‐induced lung injury. Extrapolating these findings to humans, we speculate that similar treatment with RA may reduce lung injury in preterm infants at risk for BPD. © 2004 Wiley‐Liss, Inc. © 2004 Wiley‐Liss, Inc.