The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice
- Authors
- Koh, Seong-Ho; Lee, Sang Mok; Kim, Hyun Young; Lee, Kyu-Yong; Lee, Young Joo; Kim, Hee-Tae; Kim, Juhan; Kim, Myung-Ho; Hwang, Myung Sil; Song, Chiwon; Yang, Ki-Wha; Lee, Kwang Woo; Kim, Seung Hyun; Kim, 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.
- Files in This Item
-
Go to Link
- Appears in
Collections - 서울 의과대학 > 서울 신경과학교실 > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.