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Related Experiment Videos

Molecular mechanisms contributing to necrotizing enterocolitis.

D H Chung1, R T Ethridge, S Kim

  • 1Department of Surgery, The University of Texas Medical Branch, Galveston, Texas 77555-0353, USA. dhchung@utmb.edu

Annals of Surgery
|May 24, 2001
PubMed
Summary

Necrotizing enterocolitis (NEC) involves increased cyclooxygenase-2 (COX-2) and nuclear factor-kappaB (NF-kappaB) activity. Targeting this COX-2/NF-kappaB pathway may help treat or prevent NEC in neonates.

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Area of Science:

  • Gastroenterology
  • Neonatal Medicine
  • Molecular Biology

Background:

  • Necrotizing enterocolitis (NEC) is a leading cause of neonatal mortality and morbidity.
  • The precise cellular mechanisms underlying NEC pathogenesis remain largely unknown.
  • Cyclooxygenase-2 (COX-2), regulated by nuclear factor-kappaB (NF-kappaB), is implicated in inflammatory processes.

Purpose of the Study:

  • To investigate the cellular mechanisms driving necrotizing enterocolitis (NEC) pathogenesis.
  • To determine the role of the COX-2/NF-kappaB pathway in NEC.
  • To assess COX-2 expression and NF-kappaB activity in NEC models.

Main Methods:

  • Immunohistochemistry was used to analyze COX-2 expression in human neonatal intestinal tissue with NEC.
  • A rat model of NEC was established using superior mesenteric artery occlusion and platelet-activating factor.

Related Experiment Videos

  • Western immunoblotting and gel shift assays were employed to quantify COX-2 protein and NF-kappaB binding activity.

    • Main Results:

    • Significantly elevated COX-2 protein expression was observed in all resected intestinal segments from neonates with NEC.
    • The rat NEC model demonstrated increased COX-2 protein levels and NF-kappaB binding activity.
    • A temporal correlation between COX-2 induction and NF-kappaB activation was evident in the rat model.

    Conclusions:

    • The COX-2/NF-kappaB signaling pathway is upregulated in both human NEC and an experimental rodent model.
    • These findings strongly suggest a critical role for the COX-2/NF-kappaB pathway in NEC development.
    • Targeting the COX-2/NF-kappaB pathway presents a potential therapeutic strategy for NEC prevention and treatment.