Nepalolide A inhibits the expression of inducible nitric oxide synthase by modulating the degradation of IkappaB-alpha and IkappaB-beta in C6 glioma cells and rat primary astrocytes

Br J Pharmacol. 1999 Sep;128(2):345-56. doi: 10.1038/sj.bjp.0702785.

Abstract

1 The effects of nepalolide A on the expression of inducible nitric oxide synthase (iNOS) caused by incubation with lipopolysaccharide/interferon-gamma (LPS/IFN-gamma) or tumour necrosis factor-alpha/interleukin-1beta/IFN-gamma (TNF-alpha/IL-1beta/IFN-gamma, mixed cytokines) in C6 glioma cells and primary astrocytes of rat were investigated. The mechanisms by which nepalolide A confers its effect on iNOS expression were also elucidated. 2 Treatment with LPS/IFN-gamma and mixed cytokines for 24 h elicited the induction of iNOS activity as determined by nitrite accumulation in the culture medium and assay of enzyme activity. Nepalolide A at 10 microM abrogated the LPS/IFN-gamma- and mixed cytokines-mediated induction of iNOS by more than 90% in C6 glioma cells, and by 80% for mixed cytokines-induced induction of iNOS in primary astrocytes. The effect of nepalolide A (2-10 microM) was concentration-dependent. 3 The inhibition of iNOS induction by nepalolide A was attributed to decreases in the content of iNOS protein and the level of iNOS mRNA, as measured by immunoblotting and reverse transcriptase-polymerase chain reaction. 4 Electrophoretic mobility shift assay was used to evaluate the effect of nepalolide A on the activation of nuclear factor-kappaB (NF-kappaB). Results showed that nepalolide A diminished the LPS/IFN-gamma-mediated association of NF-kappaB with consensus oligonucleotide in a concentration-dependent manner. The activation of NF-kappaB by mixed cytokines was modulated both in the extent of activation and in its time-course by nepalolide A. 5 The ability of nepalolide A to inhibit NF-kappaB activation was further confirmed by studies on the degradation of the inhibitor of NF-kappaB, IkappaB, as measured by immunoblotting. 6 The present study demonstrates that the attenuation of NF-kappaB activation by nepalolide A was mediated by blockade of the degradation of IkappaB, leading to suppression of the expression of iNOS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anthracenes / pharmacology*
  • Astrocytes / drug effects
  • Astrocytes / metabolism*
  • Biotransformation / drug effects
  • Blotting, Western
  • Brain Neoplasms / metabolism*
  • Cell Survival / drug effects
  • Cells, Cultured
  • DNA-Binding Proteins / metabolism*
  • Depression, Chemical
  • Electrophoresis
  • Enzyme Inhibitors / pharmacology*
  • Glioma / metabolism*
  • I-kappa B Proteins*
  • Interferon-gamma / antagonists & inhibitors
  • Interferon-gamma / pharmacology
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / biosynthesis
  • Nitric Oxide Synthase / antagonists & inhibitors*
  • Nitric Oxide Synthase / biosynthesis*
  • Nitric Oxide Synthase Type II
  • Nitrites / metabolism
  • Oligonucleotides / metabolism
  • Precipitin Tests
  • RNA, Messenger / biosynthesis
  • Rats
  • Rats, Sprague-Dawley
  • Recombinant Proteins

Substances

  • Anthracenes
  • DNA-Binding Proteins
  • Enzyme Inhibitors
  • I kappa B beta protein
  • I-kappa B Proteins
  • NF-kappa B
  • Nfkbia protein, rat
  • Nitrites
  • Oligonucleotides
  • RNA, Messenger
  • Recombinant Proteins
  • nepalolide A
  • NF-KappaB Inhibitor alpha
  • Interferon-gamma
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, rat