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

被引:4
作者
Lee, Hyun Ju [1 ,2 ]
Choi, Chang Won [1 ,2 ]
Kim, Beyong Il [1 ,2 ]
Kim, Ee-Kyung [2 ]
Kim, Han-Suk [2 ]
Choi, Jung-Hwan [2 ]
Lee, Myong Jin [3 ]
Yang, Eun Gyeong [3 ]
机构
[1] Seoul Natl Univ, Bundang Hosp, Dept Pediat, Songnam 463707, Gyeonggi Do, South Korea
[2] Seoul Natl Univ, Coll Med, Dept Pediat, Seoul, South Korea
[3] Korea Inst Sci & Technol, Life Sci Res Div, Seoul, South Korea
关键词
Bronchopulmonary dysplasia; chorioamnionitis; interleukin-6; protein carbonyl; vascular endothelial growth factor; ANTENATAL ENDOTOXIN; OXIDATIVE STRESS; PRETERM INFANTS; INFLAMMATION; INJURY; CHORIOAMNIONITIS; ANGIOGENESIS; INVOLVEMENT; EXPRESSION; DISEASE;
D O I
10.1515/JPM.2010.091
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
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plus hyperoxia group from day 7 to 14, whereas alveolarization resumed in the hyperoxia group after oxygen exposure was withdrawn at day 7.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 hyperoxia 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.
引用
收藏
页码:675 / 681
页数:7
相关论文
共 25 条
[1]  
Aono K, 1997, J CELL BIOCHEM, V65, P349, DOI 10.1002/(SICI)1097-4644(19970601)65:3<349::AID-JCB5>3.3.CO
[2]  
2-X
[3]   Oxidative stress in fetal lambs exposed to intra-amniotic endotoxin in a chorioamnionitis model [J].
Cheah, Fook-Choe ;
Jobe, Alan H. ;
Moss, Timothy J. ;
Newnham, John P. ;
Kallapur, Suhas G. .
PEDIATRIC RESEARCH, 2008, 63 (03) :274-279
[4]   Bronchopulmonary Dysplasia in a Rat Model Induced by Intra-amniotic Inflammation and Postnatal Hyperoxia: Morphometric Aspects [J].
Choi, Chang Won ;
Kim, Beyong Il ;
Hong, Joon-Seok ;
Kim, Ee-Kyung ;
Kim, Han-Suk ;
Choi, Jung-Hwan .
PEDIATRIC RESEARCH, 2009, 65 (03) :323-327
[5]  
Cines DB, 1998, BLOOD, V91, P3527
[6]   Endotoxin tolerance in rats:: Expression of TNF-α, IL-6, IL-10, VCAM-1 and HSP 70 in lung and liver during endotoxin shock [J].
Flohé, S ;
Fernández, ED ;
Ackermann, M ;
Hirsch, T ;
Börgermann, J ;
Schade, FU .
CYTOKINE, 1999, 11 (10) :796-804
[7]   OXYGEN-TOXICITY IN NEONATAL RATS - THE EFFECT OF ENDOTOXIN TREATMENT ON SURVIVAL DURING AND POST-O-2 EXPOSURE [J].
FRANK, L .
PEDIATRIC RESEARCH, 1987, 21 (02) :109-115
[8]  
Jobe Alan H, 2003, Semin Neonatol, V8, P9, DOI 10.1016/S1084-2756(02)00188-4
[9]   Vascular changes after intra-amniotic endotoxin in preterm lamb lungs [J].
Kallapur, SG ;
Bachurski, CJ ;
Le Cras, TD ;
Joshi, SN ;
Ikegami, M ;
Jobe, AH .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2004, 287 (06) :L1178-L1185
[10]   The clever fetus: Responding to inflammation to minimize lung injury [J].
Kramer, BW ;
Jobe, AH .
BIOLOGY OF THE NEONATE, 2005, 88 (03) :202-207