Oct 19, 2004

Neuroprotection by fructose-1,6-bisphosphate involves ROS alterations via p38 MAPK/ERK

Brain Research
Jee-Young ParkEun Joo Baik


Fructose-1,6-bisphosphate (FBP) is a glucose metabolism intermediate that shows a neuroprotective action in animal models of ischemia and other injuries. The intracellular mechanism of FBP on neuroprotection has not been previously defined. Here, we examined whether FBP has a neuroprotective effect against excitotoxicity, and whether it affects the production of reactive oxygen species (ROS), which are involved in the MAPK pathway in cortical neurons. FBP prevented neuronal death in a dose-dependent manner following 24 h of treatment with the excitotoxin, NMDA. After 8 h of NMDA treatment, we observed FBP-induced inhibition of the production of intracellular ROS, and at the earlier time FBP suppressed NMDA-induced p-p38 and p-ERK expression. In addition, MAPK inhibitors reduced NMDA-induced excitotoxicity and also ROS production. Taken together, our results suggest that the neuroprotective effects of FBP could be explained by down-regulation of free radical production through the p38MAPK/ERK pathway.

  • References42
  • Citations21


Mentioned in this Paper

ISYNA1 gene
Biochemical Pathway
MAPK3 wt Allele
Mitogen-Activated Protein Kinases
Mitogen-Activated Protein Kinase 14
Antagonist Muscle Action

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