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dc.contributor.authorLee, Hyun Ju-
dc.contributor.authorChoi, Chang Won-
dc.contributor.authorKim, Beyong Il-
dc.contributor.authorKim, Ee-Kyung-
dc.contributor.authorKim, Han-Suk-
dc.contributor.authorChoi, Jung-Hwan-
dc.contributor.authorLee, Myong Jin-
dc.contributor.authorYang, Eun Gyeong-
dc.date.accessioned2024-01-20T18:30:40Z-
dc.date.available2024-01-20T18:30:40Z-
dc.date.created2021-09-04-
dc.date.issued2010-11-
dc.identifier.issn0300-5577-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/130980-
dc.description.abstractAim: 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plus hyperoxia group from day 7 to 14, whereas alveolarization resumed in the hyperoxia group after oxygen exposure was withdrawn at day 7.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.-
dc.languageEnglish-
dc.publisherWALTER DE GRUYTER GMBH-
dc.subjectANTENATAL ENDOTOXIN-
dc.subjectOXIDATIVE STRESS-
dc.subjectPRETERM INFANTS-
dc.subjectINFLAMMATION-
dc.subjectINJURY-
dc.subjectCHORIOAMNIONITIS-
dc.subjectANGIOGENESIS-
dc.subjectINVOLVEMENT-
dc.subjectEXPRESSION-
dc.subjectDISEASE-
dc.titleSerial changes of lung morphology and biochemical profiles in a rat model of bronchopulmonary dysplasia induced by intra-amniotic lipopolysaccharide and postnatal hyperoxia-
dc.typeArticle-
dc.identifier.doi10.1515/JPM.2010.091-
dc.description.journalClass1-
dc.identifier.bibliographicCitationJOURNAL OF PERINATAL MEDICINE, v.38, no.6, pp.675 - 681-
dc.citation.titleJOURNAL OF PERINATAL MEDICINE-
dc.citation.volume38-
dc.citation.number6-
dc.citation.startPage675-
dc.citation.endPage681-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000284102500016-
dc.identifier.scopusid2-s2.0-78650134529-
dc.relation.journalWebOfScienceCategoryObstetrics & Gynecology-
dc.relation.journalWebOfScienceCategoryPediatrics-
dc.relation.journalResearchAreaObstetrics & Gynecology-
dc.relation.journalResearchAreaPediatrics-
dc.type.docTypeArticle-
dc.subject.keywordPlusANTENATAL ENDOTOXIN-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusPRETERM INFANTS-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusINJURY-
dc.subject.keywordPlusCHORIOAMNIONITIS-
dc.subject.keywordPlusANGIOGENESIS-
dc.subject.keywordPlusINVOLVEMENT-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordAuthorBronchopulmonary dysplasia-
dc.subject.keywordAuthorchorioamnionitis-
dc.subject.keywordAuthorinterleukin-6-
dc.subject.keywordAuthorprotein carbonyl-
dc.subject.keywordAuthorvascular endothelial growth factor-
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