Paper
Induction of nitric oxide synthase in macrophages: inhibition by fructose-1,6-diphosphate.
Published Feb 24, 1998 · L. Edde, X. Zhou, J. Eaton
Biochemical and biophysical research communications
22
Citations
2
Influential Citations
Abstract
Intravenous fructose-1,6-diphosphate (FDP) is reported to reverse shock and improves survival in animals given systemic lipopolysaccharide (LPS), although the mechanism is incompletely understood. Since endotoxin-related shock is associated with increased nitric oxide (NO) production, LPS-stimulated macrophages were treated with FDP, and the NO metabolite, nitrite, was measured 24 h later. Treatment of LPS-stimulated macrophages with 1, 5, or 10 mM FDP caused a dose-dependent reduction in mRNA expression for inducible NO synthase by Northern analysis and decreased the micromolar concentrations of nitrite produced by 17, 42, and 68%, respectively. Neither fructose nor sodium phosphate had these effects in LPS-exposed macrophages. Electrophoretic mobility shift assays revealed that FDP did not inhibit LPS-mediated activation of nuclear factor kappa B. Viability analysis showed that the FDP effect was not caused by cytotoxicity. Overall, these results suggest that fructose-1,6-diphosphate, a glycolytic intermediate with potential clinical use, may mitigate the adverse effects of LPS by regulating the generation of NO.
Non-RCT
Animal StudyFructose-1,6-diphosphate may mitigate the adverse effects of lipopolysaccharide by regulating nitric oxide generation in macrophages.
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