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Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes

Title
Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes
Authors
Chan Y.S.Ji W.C.Jae R.R.Kwang H.K.Choi J.-J.Kim H.-S.Lee J.-C.Lee S.J.Hyoung C.K.Kim W.-K.
Ewha Authors
김희선
SCOPUS Author ID
김희선scopus
Issue Date
2002
Journal Title
GLIA
ISSN
0894-1491JCR Link
Citation
GLIA vol. 37, no. 3, pp. 268 - 274
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
We have previously reported that the production of nitric oxide (NO) in immunostimulated astrocytes was markedly decreased under glucose-deprived conditions. The present study was undertaken to find the contributing factor(s) for the decreased NO production in glucose-deprived immunostimulated astrocytes. NO production in rat primary astrocytes was stimulated for 24-48 h by cotreatment with lipopolysaccharides (1 μg/ml) and interferon-γ (100 U/ml). Decreased NO production in immunostimulated astrocytes by glucose deprivation was mimicked by the glycolytic inhibitor 2-deoxyglucose and reversed by addition of pyruvate and lactate. Glucose deprivation did not alter the expression of inducible nitric oxide synthase (iNOS) in immunostimulated astrocytes. Addition of β-NADPH, but not tetrahydrobiopterine, both of which are essential cofactors for NOS function, completely restored the NO production that was decreased in glucose-deprived immunostimulated astrocytes. Glucose deprivation and immunostimulation synergistically reduced intracellular NADPH level in astrocytes. The results indicate that glucose deprivation decreases NO production in immunostimulated astrocytes by depleting intracellular NADPH, a cofactor of iNOS. © 2002 Wiley-Liss, Inc.
DOI
10.1002/glia.10032
Appears in Collections:
의과대학 > 의학과 > Journal papers
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