Association of Increased Pulmonary Interleukin-6 with the Priming Effect of Intra-Amniotic Lipopolysaccharide on Hyperoxic Lung Injury in a Rat Model of Bronchopulmonary Dysplasia
- Association of Increased Pulmonary Interleukin-6 with the Priming Effect of Intra-Amniotic Lipopolysaccharide on Hyperoxic Lung Injury in a Rat Model of Bronchopulmonary Dysplasia
- Do-Hyun Kim; Chang Won Choi; Ea-Kyung Kim; Han-Suk Kim; Beyong Il Kim; Jung-Hwan Choi; 이명진; 양은경
- Alveolarization; Bronchopulmonary dysplasia; Inflammation; Interleukin-6
- Issue Date
- VOL 98, NO 1, 23-32
- Results: Morphometric analysis of lung tissues demonstrated that alveolarization was significantly inhibited only in the LPS plus hyperoxia group. IL-6 [?] protein levels and its mRNA expression in the lungs were significantly increased only in the LPS plus hyperoxia group. Neither LPS nor hyperoxia increased IL-6 [?] in the lungs independently. bFGF [?] mRNA expression was significantly decreased in the LPS-treated groups. VEGF protein levels were significantly reduced by hyperoxia, whereas protein carbonyl levels were increased by intra-amniotic LPS or hyperoxia. No additional significant change to VEGF or protein carbonyl levels was produced by intra-amniotic LPS or hyperoxia. There were no significant differences in the mRNA expressions of VEGF, VEGFR-2, and TGF-beta(1). Conclusions: The priming effect of intra-amniotic LPS on hyperoxic lung injury may be associated with IL-6 [?] elevation in the lungs.
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