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. 2010 Nov;38(6):675-81.
doi: 10.1515/jpm.2010.091. Epub 2010 Aug 13.

Serial changes of lung morphology and biochemical profiles in a rat model of bronchopulmonary dysplasia induced by intra-amniotic lipopolysaccharide and postnatal hyperoxia

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Serial changes of lung morphology and biochemical profiles in a rat model of bronchopulmonary dysplasia induced by intra-amniotic lipopolysaccharide and postnatal hyperoxia

Hyun Ju Lee et al. J Perinat Med. 2010 Nov.

Abstract

Aim: to investigate serial changes of lung morphology and biochemical profiles in a rat model of bronchopulmonary dysplasia (BPD) induced by intra-amniotic lipopolysaccharide (LPS) administration and postnatal hyperoxia (85%).

Methods: we evaluated histological changes of the lungs and compared the levels of interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), and protein carbonyl in lung tissue on days 1, 7, and 14 after birth in a rat model of BPD.

Results: the inhibition of alveolarization was sustained in the LPS plus hyperoxia group from day 7 to 14, whereas alveolarization resumed in the hyperoxia group after oxygen exposure was withdrawn at day 7. Administration of LPS alone did not adversely affect lung morphometry. IL-6 levels showed transient overexpression at day 1 in the LPS-treated groups, but decreased at days 7 and 14. VEGF protein levels were elevated in the LPS-treated groups, but not in the hyper-oxia and control groups at days 1, 7, and 14. Exposure to hyperoxia affected protein carbonyl levels in the hyperoxia group at days 7 and 14.

Conclusion: lung injury induced by intra-amniotic inflammation and postnatal hyperoxia may be due to inhibition of alveolarization without recovery even after withdrawal of oxygen.

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