Potentiated glucose deprivation-induced death of astrocytes after induction of iNOS

J Neurosci Res. 1998 Dec 15;54(6):870-5. doi: 10.1002/(SICI)1097-4547(19981215)54:6<870::AID-JNR15>3.0.CO;2-3.

Abstract

Astrocytes play an essential role in the maintenance of normal neuronal function. Here we report that pretreatment of interferon-gamma (IFN-gamma) and lipopolysaccharides (LPS) made murine astrocytes highly vulnerable to glucose deprivation-induced death. Neither 12-hr glucose deprivation nor 2-day treatment with IFN-gamma (100 U/ml) and LPS (1 microg/ml) altered the viability of astrocytes. However, significant death of IFN-gamma/LPS-treated astrocytes was observed after 4-hr glucose deprivation. This augmented death was mimicked by the nitric oxide releasing reagent 3-morpholinosydnonimine and was in part prevented by the nitric oxide synthase inhibitor NG-nitroarginine. The data indicate that immunostimulated astrocytes can undergo suicidal death during glucose deprivation through the expression of inducible nitric oxide synthase.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / drug effects*
  • Astrocytes / enzymology
  • Cell Death / drug effects*
  • Culture Media
  • Enzyme Induction
  • Glucose / administration & dosage*
  • Glucose / metabolism
  • Interferon-gamma / pharmacology*
  • Lipopolysaccharides / pharmacology*
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase / metabolism*
  • Nitric Oxide Synthase Type II
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Culture Media
  • Lipopolysaccharides
  • Nitric Oxide
  • Interferon-gamma
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, rat
  • Glucose