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

Young Shin Chan, Woong Choi Ji, Ryun Ryu Jae, Ho K. Kwang, Jung J. Choi, Hyun S. Kim, Hee S. Kim, Jae Chul Lee, Sun Jung Lee, Chun Kim Hyoung, Won-Ki Kim

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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.

Original languageEnglish
Pages (from-to)268-274
Number of pages7
JournalGLIA
Volume37
Issue number3
DOIs
Publication statusPublished - 2002 Mar 1
Externally publishedYes

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Keywords

  • Cell death
  • Cofactor
  • Glutathione
  • iNOS
  • Tetrahydrobiopterine

ASJC Scopus subject areas

  • Immunology

Cite this

Chan, Y. S., Ji, W. C., Jae, R. R., Kwang, H. K., Choi, J. J., Kim, H. S., Kim, H. S., Lee, J. C., Lee, S. J., Hyoung, C. K., & Kim, W-K. (2002). Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes. GLIA, 37(3), 268-274. https://doi.org/10.1002/glia.10032