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Caffeine Protects Against Hyperoxia-Induced Structural Lung Injury and Restores Alveolar Development in Neonatal

Stefanie Endesfelder1, Christoph Bührer1

  • 1Department of Neonatology, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany.

Antioxidants (Basel, Switzerland)
|December 30, 2025
PubMed
Summary
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Caffeine mitigates lung damage in a neonatal rat model of bronchopulmonary dysplasia (BPD) by reducing oxidative stress and normalizing gene expression. Further research is needed to determine optimal caffeine dosing for lung injury recovery.

Area of Science:

  • Neonatal Medicine
  • Pulmonary Biology
  • Pharmacology

Background:

  • Oxidative stress from hyperoxia is a key factor in neonatal lung injury and bronchopulmonary dysplasia (BPD).
  • The immature lung's developing antioxidant defenses make it vulnerable to damage during high-oxygen exposure.
  • Disrupted alveolar and vascular maturation contribute to BPD pathogenesis.

Purpose of the Study:

  • To investigate the protective effects of caffeine on hyperoxia-induced neonatal lung injury in a rat model.
  • To determine caffeine's impact on lung architecture, gene expression, and fibrotic signaling pathways.

Main Methods:

  • A rat model of BPD was established using 80% oxygen exposure for 3-5 days.
  • Lung injury was assessed via histological staining (Sirius Red, toluidine blue) and morphometric analysis.
Keywords:
caffeinefibrosishyperoxiamorphologyoxygenpostnatal immature lung

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  • Gene expression related to angiogenesis and fibrosis was quantified, along with fibrogenic signaling pathways (TGF-β/CTGF).

    • Main Results:

    • Hyperoxia induced simplified alveolar architecture, reduced angiogenesis, and increased collagen deposition.
    • Caffeine treatment mitigated structural lung damage and normalized the expression of key angiogenic and fibrotic genes.
    • Caffeine counteracted TGF-β/CTGF signaling, promoting lung recovery, although it transiently upregulated profibrotic mediators under normoxia.

    Conclusions:

    • Caffeine demonstrates antioxidant and antifibrotic properties, mitigating hyperoxia-induced lung injury in neonatal rats.
    • Caffeine may promote physiological lung maturation, suggesting potential therapeutic benefits for BPD.
    • Further studies are warranted to optimize caffeine dosage and understand its context-dependent effects on fibrotic signaling for clinical translation.