β-funaltrexamine inhibits inducible nitric-oxide synthase expression in human astroglial cells

Randall L. Davis, Daniel J. Buck, Neda Saffarian, Shekher Mohan, Udaya DeSilva, Samodha C. Fernando, Craig W. Stevens

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

The inducible isoform of nitric-oxide synthase (iNOS) is involved in neuropathogenesis associated with infection and disease in the brain. Hence, there is considerable interest in the identification of therapeutic interventions to prevent iNOS-mediated pathology. Astroglia are a major site of iNOS expression during neuropathogenesis. To mimic a key component of neuroinflammation, human A172 astroglial cells were exposed in vitro to a cytokine mixture containing interferon γ, tumor necrosis factor α, and interleukin-1β, resulting in significant iNOS expression. Next, we assessed the effects of the mu opioid receptor antagonist, β-funaltrexamine (β-FNA), on cytokine induced iNOS expression in human astroglia. β-FNA dose-dependently inhibited iNOS expression. β-FNA transcriptionally (or pre-transcriptionally) inhibited cytokine-induced iNOS activation as indicated by a significant decrease in NOS2 messenger RNA expression. Further characterization of the novel, anti-inflammatory actions of β-FNA may provide insights for pharmacologic strategies to treat or prevent brain pathologies associated with neuroinflammation.

Original languageEnglish
Pages (from-to)150-153
Number of pages4
JournalJournal of Neuroimmune Pharmacology
Volume3
Issue number3
DOIs
StatePublished - Sep 2008

Keywords

  • Astrocytes
  • Fentanyl
  • Morphine
  • Neuroinflammation
  • Nitric oxide
  • Opioids

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