ArticleJournal of neuroinflammation2025
Prenatal inflammation exacerbates hyperoxia-induced neonatal brain injury.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Article
- Dexmedetomidine Preserves Hippocampal Neurogenesis During Recovery from Neonatal Hyperoxia in Rats.Cells · 2026Article
- Advances in Perinatal Depression: A Focus on Screening and Treatment.Journal of clinical medicine · 2026Review
- Intracranial LPS injection induces cerebral palsy-like motor and behavioral deficits in immunodeficient mice.Scientific reports · 2026Article
- Risk factors for developmental delays in small for gestational age children at age of 24-36 months.European child & adolescent psychiatry · 2026Article
- MiR-181a, IL-6, and TNF-α: Biomarkers for Diagnosis and Long-Term Neurodevelopmental Prognosis in Neonatal Sepsis.Infection and drug resistance · 2026Article
- Developmentally sensitive neuropharmacological effects of dexamethasone in neonatal bronchopulmonary dysplasia-associated brain injury via microglial Acod1-itaconate/IL-1β signaling.Frontiers in pharmacology · 2026Article
- Therapeutic effect and mechanism of different doses of aspirin on preterm delivery in pregnant mice.PloS one · 2026Article
- Predicting Neonatal Morbidity and Correlations with Maternal and Neonatal Biomarkers in Connection with Fetal Inflammatory Response Syndrome in Premature Births.Journal of clinical medicine · 2025Article
- Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.Antioxidants (Basel, Switzerland) · 2025Review
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10 authors.
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Abstract
backgroundPremature born infants are at high risk to develop white matter injury (WMI). Hyperoxia and perinatal inflammation are main risk factors for preterm birth and associated brain injury. To date the majority of experimental studies have focused on isolated insults. However, clinically, WMI injury is a multifactorial disorder caused by a variety of triggers. To establish a clinically relevant rodent model of WMI, we combined prenatal inflammation with postnatal hyperoxia to investigate individual, and additive or synergistic effects on inflammatory processes, myelination and grey matter development.
methodsAt embryonic day 20, pregnant Wistar rat dams received either a single intraperitoneal injection of 100 µg/ kg lipopolysaccharide (LPS) or sodium chloride. Offspring were either exposed to hyperoxia (80% O
resultsPrenatal inflammation combined with postnatal hyperoxia resulted in reduced body weight and length in the offspring, accompanied by increased serum leptin levels at term equivalent age. The altered body parameters, like body weight, were associated with decreased brain volume, thinning of deep cortical layers and hypomyelination. As potential underlying mechanisms, we identified severe myelination deficits and an increased microglia activation associated with elevated inflammatory cytokine expression in brain tissues, while peripheral cytokine levels were reduced. Interestingly, effects on body size were mainly mediated by prenatal LPS, independent of hyperoxia, while oligodendrocyte degeneration was mainly induced by postnatal hyperoxia, independent of prenatal inflammation. However, for the majority of pathological changes, including brain size, myelination deficits, microglia activation and inflammatory cytokine expression, additive or synergistic effects were detected.
conclusionPrenatal inflammation combined with postnatal hyperoxia results in aggravated myelination deficits and inflammatory responses compared to single insults, making it an ideal model to improve our understanding of the complex pathophysiology underlying WMI and to evaluate urgently needed therapies.
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