Budesonide epimer R, LAU-8080 and phenyl butyl nitrone synergistically repress cyclooxygenase-2 induction in [IL-1β + Aβ42]-stressed human neural cells

Merete Boedker, Anja Boetkjaer, Nicolas G. Bazan, Jian Guo Cui, Yuhai Zhao, Ricardo Palacios Pelaez, Walter J. Lukiw

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Interleukin-1beta (IL-1β) and amyloid-beta peptide 42 (Aβ42) together induce a robust proinflammatory gene expression program in human neural cells in primary culture. One consistent genetic marker for this triggered inflammatory response is an increase in the expression of cycloooxygenase-2 (COX-2), a prostaglandin synthase also found to be up-regulated in neurological disorders such as Alzheimer's disease. In this study we provide data illustrating the combined effect of three independent classes of compounds: the glucocorticoid budesonide epimer R, the platelet-activating factor antagonist LAU-8080, and the free radical scavenger phenyl butyl nitrone, upon COX-2 gene activation and prostaglandin E2 (PGE2) levels in [IL-1β + Aβ42]-stressed HN cells. The data indicate that specific combinations of repressors of COX-2 activity are synergistic in modulating the stress-induced up-regulation of COX-2 and PGE2, and this may be of potential therapeutic value in the design of treatment for complex neuroinflammatory disorders.

Original languageEnglish (US)
Pages (from-to)176-180
Number of pages5
JournalNeuroscience Letters
Volume380
Issue number1-2
DOIs
StatePublished - May 20 2005

Keywords

  • Alzheimer's disease model
  • Budesonide epimer R
  • Combinatorial drug cocktails
  • COX-2 inhibition
  • Cyclooxygenase-2
  • Human neural cells
  • LAU-8080
  • Neuroinflammation
  • Phenyl butyl nitrone
  • Prostaglandin E

ASJC Scopus subject areas

  • Neuroscience(all)

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