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

• Published in: Journal of neuroscience research 1998-12, Vol.54 (6), p.870-875
• Main Authors: Choi, Jung-Jin, Kim, Won-Ki
• Format: Article
• Language: English
• Subjects: Animals; astrocyte; Astrocytes - drug effects; Astrocytes - enzymology; Cell Death - drug effects; Culture Media; Enzyme Induction; Glucose - administration & dosage; Glucose - metabolism; glucose deprivation; immunostimulation; Interferon-gamma - pharmacology; ischemia; Lipopolysaccharides - pharmacology; nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase - metabolism; Nitric Oxide Synthase Type II; Rats; Rats, Sprague-Dawley
• ISSN: 0360-4012; 1097-4547
• DOI: 10.1002/(SICI)1097-4547(19981215)54:6<870::AID-JNR15>3.0.CO;2-3

Astrocytes play an essential role in the maintenance of normal neuronal function. Here we report that pretreatment of interferon‐γ (IFN‐γ) and lipopolysaccharides (LPS) made murine astrocytes highly vulnerable to glucose deprivation‐induced death. Neither 12‐hr glucose deprivation nor 2‐day treatment with IFN‐γ (100 U/ml) and LPS (1 μg/ml) altered the viability of astrocytes. However, significant death of IFN‐γ/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. J. Neurosci. Res. 54:870–875, 1998.  © 1998 Wiley‐Liss, Inc.