Oct 19, 2004

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

Brain Research
Jee-Young ParkEun Joo Baik

Abstract

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

Citations

Mentioned in this Paper

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

Related Feeds

Astrocytes and Neurodegeneration

Astrocytes are important for the health and function of the central nervous system. When these cells stop functioning properly, either through gain of function or loss of homeostatic controls, neurodegenerative diseases can occur. Here is the latest research on astrocytes and neurodegeneration.