title: [Effects of glucocorticoid on RAGE-NF-κB pathway in hyperoxia-induced lung tissues of neonatal rats].
abstract: OBJECTIVE
  To explore the change of RAGE-NF-κB signaling pathway during the course of hyperoxia-induced lung injury in newborn rats, and the effect of glucocorticoid on this pathway.
  
  
  METHODS
  Twenty-four Sprague-Dawley neonatal rats were randomly divided into three groups (n=8 each) : sham control (control group), hyperoxia-induced acute lung injury (model group) and glucocorticoid-treated acute lung injury (glucocorticoid group). Rats were sacriﬁced at 13 days after birth. RAGE and NF-κB expression levels in lung tissues were detected by reverse transcription polymerase chain reaction, Western blot and immunohistochemistry analysis. The levels of tumor necrosis factor α (TNF-α) and sRAGE in bronchoalveolar lavage ﬂuid (BALF) and serum were measured using ELISA. Lung damage was evaluated by histological examinations.
  
  
  RESULTS
  RAGE and NF-κB mRNA and protein expression levels in lung tissues were signiﬁcantly increased in the model and glucocorticoid groups compared with the control group (P<0.05). Serum RAGE concentrations were signiﬁcantly increased but RAGE concentrations in BALF were significantly reduced in the model and glucocorticoid groups compared with the control group (P<0.05). RAGE and NF-κB expression at both mRNA and protein levels in lung tissues was signiﬁcantly lower in the glucocorticoid group than in the model group (P<0.05). RAGE concentrations were signiﬁcantly lower in serum (P<0.05), but were higher in BALF (P<0.05) in the glucocorticoid group than in the model group.
  
  
  CONCLUSIONS
  RAGE-NF-κB pathway plays an important role in hyperoxia-induced lung injury in neonatal rats, and glucocorticoid administration may play a protective role against the lung injury by down-regulating RAGE-NF-κB signaling pathway.
authors.affiliation: Department of Neonatology, Huai'an First Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, China. lyh0729@163.com.
authors.forename: Jian
authors.initials: J
authors.lastname: Hu
authors.forename: Min
authors.initials: M
authors.lastname: Yu
authors.forename: Yun
authors.initials: Y
authors.lastname: Tang
authors.forename: Zhao-Fang
authors.initials: ZF
authors.lastname: Tian
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D005938:Glucocorticoids / Q000494:pharmacology*; D018496:Hyperoxia / Q000150:complications*; D055370:Lung Injury / Q000517:prevention & control*; D016328:NF-kappa B / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D005938:Glucocorticoids; D016328:NF-kappa B; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha