Glycine inhibits ethanol-induced oxidative stress, neuroinflammation and apoptotic neurodegeneration in postnatal rat brain
- Authors
- Amin, Faiz Ul; Shah, Shahid Ali; Kim, Myeong Ok
- Issue Date
- Jun-2016
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- Ethanol; Glycine; Apoptotic neurodegeneration; Neuroprotection; FAS
- Citation
- NEUROCHEMISTRY INTERNATIONAL, v.96, pp.1 - 12
- Indexed
- SCIE
SCOPUS
- Journal Title
- NEUROCHEMISTRY INTERNATIONAL
- Volume
- 96
- Start Page
- 1
- End Page
- 12
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/15476
- DOI
- 10.1016/j.neuint.2016.04.001
- ISSN
- 0197-0186
- Abstract
- Here we investigated for the first time the inhibitory potential of Glycine (Gly) against ethanol-induced oxidative stress, neuroinflammation and apoptotic neurodegeneration in human neuroblastoma SH-SY5Y cells and in the developing rat brain. The Gly co-treatment significantly increased the cell viability, inhibited the expression of phospho-Nuclear Factor kappa B (p-NF-kappa B) and caspase-3 and reduced the oxidative stress in ethanol-treated SH-SY5Y cells in a PI3K-dependent manner. Seven days old male rat pups were injected with ethanol (5 g/kg subcutaneously, prepared in a 20% saline solution) and Gly (1 g/kg). Gly co-treatment stimulated the PI3K/Alct signaling pathway to limit the ethanol induced reactive oxygen species (ROS) production in the developing rat brain. It lowered the ethanol-elevated levels of phospho-c Jun N terminal kinase (p-JNK) and its various downstream apoptotic markers, including Bax, cytochrome C, caspase-3 and PARP-1. Additionally, the Gly treatment upregulated antiapoptotic Bcl-2 proteins and prevented ethanol-induced neurodegeneration as assessed by Fluoro-Jade-B (FJB) and Nissl staining. Furthermore, the Gly administration caused significant reduction in the ethanol-induced neuroinflammation by inhibiting the expression of inflammatory markers such as p-NF-kappa B, cyclooxygenase 2 (COX2) and tumor necrosis factor-alpha (TNF-alpha) and reversed the ethanol-induced synaptic protein markers expression. The results suggest that acute Gly treatment reduces ethanol-induced oxidative stress and neuronal cell loss in SH-SY5Y cells and in the developing rat brain. Therefore, Gly may be considered as potential treatment in ethanol-intoxicated newborns and infants. (C) 2016 Elsevier Ltd. All rights reserved.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - ETC > Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.gnu.ac.kr/handle/sw.gnu/15476)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.