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Chinese Journal of Contemporary Pediatrics ; (12): 1149-1153, 2014.
Article Dans Chinois | WPRIM | ID: wpr-289514

Résumé

<p><b>OBJECTIVE</b>To study the expression of fatty acid binding protein 4 (FABP4) in lungs and bronchoalveolar lavage fluid (BALF) of preterm rats exposed to 60% O2 and to elucidate the relationship between the changes of FABP4 expression and the pathogenesis of bronchopulmonary dysplasia (BPD).</p><p><b>METHODS</b>Hyperoxic lung injury was induced by exposing to 60% O2 in Spraque-Dawley rats within 6 hours after birth. Rats exposed to air were used as the control group. The lungs from groups aged postnatal days 3, 7 and 14 were removed and dissected from the main bronchi for analysis. Eight rats of each group were used to assess expression of FABP4 in lungs by immunohistochemistry and ELISA. Lung FABP4 mRNA levels were measured by semi-quantitative reverse transcription polymerase chain reaction. The levels of FABP4 in BALF were measured using ELISA.</p><p><b>RESULTS</b>FABP4 immunoreactivity was detected in the majority of alveolar macrophages, bronchial epithelial cells and endothelial cells. FABP4 protein levels in lung tissues in the hyperoxic exposure group increased significantly compared with the control group on days 3, 7 and 14 after birth (P<0.05), and FABP4 mRNA levels in lung tissues also increased significantly in the hyperoxic exposure group compared with the control group on days 7 and 14 after birth (P<0.05). The hyperoxic exposure group demonstrated increased FABP4 levels in BALF compared with the control group on days 7 and 14 after birth (P<0.05).</p><p><b>CONCLUSIONS</b>FABP4 levels increase in preterm rat lungs after hyperoxic lung injury, which may contribute to the pathogenesis of BPD.</p>


Sujets)
Animaux , Femelle , Mâle , Rats , Dysplasie bronchopulmonaire , Protéines de liaison aux acides gras , Génétique , Hyperoxie , Métabolisme , Poumon , Chimie , Lésion pulmonaire , Métabolisme , ARN messager , Rat Sprague-Dawley , Facteur de croissance endothéliale vasculaire de type A , Physiologie
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