Brain-derived neurotropic factor prevents superoxide anion-induced death of PC12h cells stably expressing TrkB receptor via modulation of reactive oxygen species

Neurosci Res. 1999 Oct;35(1):9-17. doi: 10.1016/s0168-0102(99)00062-0.


In our previous report (Satoh et al., 1999. Regulation of reactive oxygen species by nerve growth factor but not by Bcl-2 as a novel mechanism of protection of PC12 cells from superoxide anion-induced death. J. Biochem. 125, 952-959), we reported that nerve growth factor (NGF) protected PC12 cells from superoxide anion (O2-)-induced cell death through a novel regulation of reactive oxygen species (ROS) which increased O2- and decreased hydrogen peroxide (H2O2), indicating that decreasing conversion from O2- to H2O2 is a critical process for the protection by NGF. In the present study, we performed a comparative study on protective mechanisms between NGF and brain-derived neurotrophic factor (BDNF) using TrkB-expressing PC12h cells. When compared with NGF, BDNF induced a weaker but significant protective effect on the cells from O2- induced death. BDNF did not seem to change the total amount of ROS in the cells treated with xanthine and xanthine oxidase. On the other hand, BDNF increased O2- and decreased H2O2- levels in the same cells, although not so strongly as NGF. These results suggest that decreasing conversion from O2- to H2O2 is also critical for the protection by BDNF, which is considered to play a central role in survival and differentiation of CNS neurons.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain-Derived Neurotrophic Factor / pharmacology*
  • Brain-Derived Neurotrophic Factor / physiology
  • Cell Death / drug effects
  • Cell Survival / drug effects
  • Fluorescent Dyes
  • Kinetics
  • Microscopy, Fluorescence
  • Nerve Growth Factors / pharmacology
  • Nerve Growth Factors / physiology
  • Neuroprotective Agents / pharmacology
  • PC12 Cells
  • Rats
  • Reactive Oxygen Species / physiology*
  • Receptor, trkB / physiology*
  • Recombinant Proteins / metabolism
  • Recombinant Proteins / pharmacology
  • Superoxides / metabolism*
  • Transfection
  • Xanthine / toxicity
  • Xanthine Oxidase / toxicity


  • 2.5S nerve growth factor
  • Brain-Derived Neurotrophic Factor
  • Fluorescent Dyes
  • Nerve Growth Factors
  • Neuroprotective Agents
  • Reactive Oxygen Species
  • Recombinant Proteins
  • Superoxides
  • Xanthine
  • Xanthine Oxidase
  • Receptor, trkB