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Alpha-phenyl-N-tert-butylnitrone attenuates hyperoxia-induced lung injury by down-modulating inflammation in neonatal rats.

Abstract
This study was done to determine whether alpha -phenyl-N-tert-butylnitrone (PBN), a spin-trapping agent possessing significant anti-inflammatory capabilities, could attenuate hyperoxia-induced lung injury, and if so, whether this protective effect is mediated by the down-modulation of inflammation in neonatal rats. Newborn Sprague-Dawley rat pups were subjected to 14 days of hyperoxia (> 90% oxygen) within 10 hours after birth. PBN treatment, given 100 mg/kg intraperitoneally daily throughout the experiment, significantly attenuated hyperoxia-induced lung pathology, such as decreased radial alveolar count, increased mean linear intercept, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling-positive cells. Hyperoxia-induced activation of nicotinamide adenine dinucleotide phosphate oxidase that is responsible for superoxide anion production, as evidenced by up-regulation and membrane translocation of p67phox, and the inflammatory responses, such as increased mRNA expression of tumor necrosis factor-alpha, interleukin-6, and transforming growth factor-beta, were also significantly attenuated with PBN treatment. In summary, a spin-trapping agent PBN significantly attenuated hyperoxia-induced lung injury by down-regulating the inflammatory responses in neonatal rats.
AuthorsYun Sil Chang, Yu Jin Kim, Hye Soo Yoo, Dong Kyung Sung, Soo Yoon Kim, Saem Kang, Won Soon Park
JournalExperimental lung research (Exp Lung Res) Vol. 35 Issue 3 Pg. 234-49 (Apr 2009) ISSN: 1521-0499 [Electronic] England
PMID19337906 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cyclic N-Oxides
  • Cytokines
  • Free Radical Scavengers
  • Phosphoproteins
  • RNA, Messenger
  • neutrophil cytosol factor 67K
  • phenyl-N-tert-butylnitrone
Topics
  • Animals
  • Animals, Newborn
  • Cyclic N-Oxides (pharmacology, therapeutic use)
  • Cytokines (genetics)
  • Free Radical Scavengers (pharmacology, therapeutic use)
  • Gene Expression Regulation
  • Hyperoxia (pathology)
  • Inflammation (drug therapy)
  • Lung Injury (drug therapy, etiology, pathology)
  • Phosphoproteins (genetics)
  • RNA, Messenger (analysis)
  • Rats
  • Rats, Sprague-Dawley

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