ArticleScientific reports2023
The severity of NEC is ameliorated by prostaglandin E2 through regulating intestinal microcirculation.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- Severe anemia in preterm infants associated with increased bacterial virulence potential and metabolic disequilibrium.Pediatric research · 2025Article
- Pain management in preterm infants with necrotizing enterocolitis: an international expert consensus statement.European journal of pediatrics · 2025Article
- Comprehensive Characterization of the Oxidative Stress Profiles in Neonatal Necrotizing Enterocolitis.International journal of medical sciences · 2025Article
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Authors and funding
9 authors at 3 institutions in 1 country.
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Abstract
Prostaglandin E2 (PGE2) is implicated in intestinal inflammation and intestinal blood flow regulation with a paradoxical effect on the pathogenesis of necrotizing enterocolitis (NEC), which is not yet well understood. In the current study, we found that PGE2, EP4, and COX-2 varied at different distances from the most damaged area in the terminal ileum obtained from human infants with NEC. PGE2 administration alleviated the phenotype of experimental NEC and the intestinal microvascular features in experimental NEC, but this phenomenon was inhibited by eNOS depletion, suggesting that PGE2 promoted intestinal microcirculatory perfusion through eNOS. Furthermore, PGE2 administration increased the VEGF content in MIMECs under TNFα stress and promoted MIMEC proliferation. This response to PGE2 was involved in eNOS phosphorylation and nitric oxide (NO) production and was blocked by the EP4 antagonist in vitro, suggesting that targeting the PGE2-EP4-eNOS axis might be a potential clinical and therapeutic strategy for NEC treatment. The study is reported in accordance with ARRIVE guidelines ( https://arriveguidelines.org ).
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