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The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice

Authors
Koh, Seong-HoLee, Sang MokKim, Hyun YoungLee, Kyu-YongLee, Young JooKim, Hee-TaeKim, JuhanKim, Myung-HoHwang, Myung SilSong, ChiwonYang, Ki-WhaLee, Kwang WooKim, Seung HyunKim, Ok-Hee
Issue Date
Mar-2006
Publisher
ELSEVIER IRELAND LTD
Keywords
ALS; EGCG; transgenic mouse; neuronal cell death
Citation
NEUROSCIENCE LETTERS, v.395, no.2, pp.103 - 107
Indexed
SCIE
SCOPUS
Journal Title
NEUROSCIENCE LETTERS
Volume
395
Number
2
Start Page
103
End Page
107
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/181691
DOI
10.1016/j.neulet.2005.10.056
ISSN
0304-3940
Abstract
Epigallocatechin gallate (EGCG) is a constituent of green tea, and increasing evidence suggests that EGCG has neuroprotective effects on oxidative stress-injured neuronal cells, especially motoneurons. Although the neuroprotective effects of EGCG have been demonstrated in Parkinson's and Alzheimer's diseases and ischemic stroke models, there has been no report on the effect of EGCG on an in vivo model of amyotrophic lateral sclerosis (ALS). This study was undertaken to evaluate the effect of EGCG on ALS model mice with the human G93A mutated Cu/Zn-superoxide dismutase (SOD1) gene. We treated each group of 11 ALS model mice with EGCG (1.5, 2.9, and 5.8 mu g/g body weight), dissolved in 0.5 ml of 0.9% sterile NaCl, and one group of 11 with 0.5 ml of 0.9% sterile NaCl (control group) intraorally every day after 60 days of age (presymptomatic treatment). The treatment of more than 2.9 mu g EGCG/g body weight significantly prolonged the symptom onset and life span, preserved more survival signals, and attenuated death signals. These data suggest that EGCG could be a potential therapeutic candidate for ALS as a disease-modifying agent.
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