作者: Patricia Vosdoganes , Rebecca Lim , Eugenia Koulaeva , Siow Teng Chan , Rutu Acharya
DOI: 10.1016/J.JCYT.2013.03.004
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摘要: Abstract Background aims Human amnion epithelial cells (hAECs) prevent pulmonary inflammation and injury in fetal sheep exposed to intrauterine lipopolysaccharide. We hypothesized that hAECs would similarly mitigate hyperoxia-induced neonatal lung injury. Methods Newborn mouse pups were randomized either normoxia (inspired O 2 content (FiO ) = 0.21, n = 60) or hyperoxia 0.85, 57). On postnatal days (PND) 5, 6 7, sterile saline (control) was administered intraperitoneally. All animals assessed at PND 14. Results Hyperoxia associated with inflammation, alveolar simplification reduced growth. Administration of hyperoxia-exposed mice normalized body weight significantly attenuated some aspects (mean linear intercept septal crest density) (interleukin-1α, interleukin-6, transforming growth factor-β platelet-derived factor-β). However, did not alter changes airspace volume, tissue tissue-to-airspace ratio, collagen leukocyte infiltration induced by hyperoxia. Conclusions Intraperitoneal administration partially structural damage. These observations suggest may be a potential therapy for disease.