Effect of Bee Venom on Glutamate-mediated Excitotoxicity in NSC-34 Motor Neuronal Cells

Glutamate 매개 흥분성 신경독성에 대한 봉독의 NSC-34 신경세포사멸 억제 효과

  • Lee, Sang-Min (Department of Standard Research, Korea Institute of Oriental Medicine) ;
  • Choi, Sun-Mi (Department of Standard Research, Korea Institute of Oriental Medicine) ;
  • Jung, So-Young (Department of Standard Research, Korea Institute of Oriental Medicine) ;
  • Yang, Eun-Jin (Department of Standard Research, Korea Institute of Oriental Medicine)
  • 이상민 (한국한의학연구원 표준화 연구 본부) ;
  • 최선미 (한국한의학연구원 표준화 연구 본부) ;
  • 정소영 (한국한의학연구원 표준화 연구 본부) ;
  • 양은진 (한국한의학연구원 표준화 연구 본부)
  • Received : 2011.08.11
  • Accepted : 2011.09.02
  • Published : 2011.10.31

Abstract

Bee venom (BV), which is extracted from honeybees, has been used in traditional Korean medical therapy. Glutamate-mediated excitotoxicity contributes to neuronal death in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) or Alzheimer's disease (AD). This study is to investigate the effect of BV on glutamate-induced neurotoxicity on NSC-34 motor neuron cells. To determine the viability of motor neuronal cells, we performed with MTT assays in glutamate-treated NSC-34 cell with BV or without. For the measurement of oxidative stress, DCF assay was used in glutamate-treated NSC-34 motor neuronal cells with BV or without. To investigate the molecular mechanism of BV against glutamate-mediated neurotoxicity in NSC-34 cells, western blot analysis was used. Glutamate significantly decreased cell viability by glutamate dose- or treatment time-dependent manner in NSC-34 cells. However, BV pre-treatment dramatically inhibited glutamate-induced neuronal cell death. Furthermore, we found that BV increased the expression of Bcl-2 protein that is anti-apoptotic protein and reduced the generation of oxidative stress. BV has a neuroprotective role against glutamate neurotoxicity by an increase of anti-apoptotic protein. It suggests that BV may be useful for the reduction of neuronal cell death in neuronal disease models.

Keywords

References

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