{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T03:01:45Z","timestamp":1782961305592,"version":"3.54.5"},"reference-count":44,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2024,5,21]],"date-time":"2024-05-21T00:00:00Z","timestamp":1716249600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Pediatric Pulmonology"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Bronchopulmonary dysplasia (BPD) is the most common chronic morbidity in extremely preterm infants. Mesenchymal stem cells\u2010derived exosomes (MSC\u2010Exos) therapies have shown prospects in animal models of BPD. Our study aimed to evaluate the effect of adipose mesenchymal stem cells\u2010derived exosomes (AMSC\u2010Exos) on BPD and the role of the\u00a0NF\u2010\u03baB signaling pathway in this process.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The AMSCs\u00a0were extracted and AMSC\u2010Exos were isolated by ultracentrifugation method. Newborn rats were exposed to hyperoxia (90% O<jats:sub>2<\/jats:sub>) continuously for 7 days to establish a BPD model. The rats were treated with AMSC\u2010Exos by intratracheal administration on postnatal day 4 (P4). Pulmonary morphology, pulmonary vasculature, inflammatory factors, and NF\u2010\u03baB were assessed. Hyperoxia\u2010induced primary type II alveolar epithelial cells (AECIIs) and AMSC\u2010Exos treatment with or without a pan\u2010NF\u2010\u03baB inhibitor (PDTC) were established to explore the potential mechanism.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Hyperoxia\u2010exposed rats showed alveolar simplification with decreased radial alveolar count\u00a0and increased mean linear intercept,\u00a0low CD31, and vascular endothelial growth factor\u00a0expression, reduced microvessel density, increased the expression of TNF\u2010\u03b1, IL\u20101\u03b2, and IL\u20106 and decreased the expression of IL\u201010, and induced NF\u2010\u03baB phosphorylation. AMSC\u2010Exos protected the neonatal lung from the hyperoxia\u2010induced arrest of alveolar and vascular development, alleviated inflammation, and inhibited NF\u2010\u03baB phosphorylation. Hyperoxia decreased viability, increased apoptosis, enhanced inflammation, and induced NF\u2010\u03baB phosphorylation of AECIIs but improved by AMSC\u2010Exos, PDTC, or AMSC\u2010Exos+PDTC. The effect of AMSC\u2010Exos+PDTC in AECIIs was the same as AMSC\u2010Exos, but more notable than PDTC alone.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>AMSC\u2010Exos attenuated the hyperoxia\u2010induced lung injury in neonatal rats by inhibiting the NF\u2010\u03baB signaling pathway partly.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ppul.27057","type":"journal-article","created":{"date-parts":[[2024,5,21]],"date-time":"2024-05-21T13:55:18Z","timestamp":1716299718000},"page":"2523-2534","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Adipose mesenchymal stem cells\u2010derived exosomes attenuated hyperoxia\u2010induced lung injury in neonatal rats via inhibiting the NF\u2010\u03baB signaling 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