Neurochemical Research

, Volume 31, Issue 10, pp 1263–1269

Neuroprotective Effects of (-)-Epigallocatechin-3-gallate in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

  • Zhihao Xu
  • Sheng Chen
  • Xuping Li
  • Guangrui Luo
  • Liang Li
  • Weidong Le
Original Paper

DOI: 10.1007/s11064-006-9166-z

Cite this article as:
Xu, Z., Chen, S., Li, X. et al. Neurochem Res (2006) 31: 1263. doi:10.1007/s11064-006-9166-z

Abstract

The purpose of this study is to evaluate neuroprotective effects of (-)-Epigallocatechin-3-gallate (EGCG) in a transgenic mouse model of Amyotrophic lateral sclerosis (ALS). SOD1-G93A transgenic mice and wild-type mice were randomly divided into EGCG-treated groups (10 mg/kg, p.o) and vehicle-treated control groups. Rotarod measurement was performed to assess the motor function of mice starting at the age of 70 days. Nissl staining to examine the number of motor neurons and CD11b immunohistochemical staining to evaluate activation of microglia in the lumbar spinal cords were conducted at the age of 120 days. In addition, for further observation of regulation of cell signaling pathways by EGCG, we used immunohistochemical analysis for nuclear factor kappa B (NF-κB) and cleaved caspase-3 as well as western blot analysis to determine the expression of nitric oxide synthase (iNOS) and NF-κB in the spinal cord. This study demonstrated that oral administration of EGCG beginning from a pre-symptomatic stage significantly delayed the onset of disease, and extended life span. Furthermore, EGCG-treated transgenic mice showed increased number of motor neurons, diminished microglial activation, reduced immunohistochemical reaction of NF-κB and cleaved caspase-3 as well as reduced protein level of iNOS and NF-κB in the spinal cords. In conclusion, this study provides further evidences that EGCG has multifunctional therapeutic effects in the mouse model of ALS.

Keywords

Amyotrophic lateral sclerosis Cu/Zn superoxide dismutase (-)-Epigallocatechin-3-gallate Neuroprotection 

Copyright information

© Springer Science+Business Media, LLC 2006

Authors and Affiliations

  • Zhihao Xu
    • 1
  • Sheng Chen
    • 2
  • Xuping Li
    • 1
  • Guangrui Luo
    • 1
  • Liang Li
    • 1
  • Weidong Le
    • 1
    • 2
  1. 1.Institute of Health Sciences, Shanghai Institutes for Biological SciencesChinese Academy of Sciences & Shanghai Jiao Tong University School of MedicineShanghaiP. R. China
  2. 2.Institute of Neurology, Ruijin HospitalJiao Tong University School of MedicineShanghaiP. R. China

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