Abstract |
Oxidative stress and/or low cellular glutathione are associated with development and progression of neurodegenerative diseases. We have shown that S-allylmercapto-N-acetylcysteine (ASSNAC) up-regulates the level of glutathione and phase II detoxifying enzymes in cultured vascular endothelial cells. The present study demonstrates that exposure of nerve cell lines to ASSNAC significantly increases the cellular level of glutathione probably via activation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and protects the cells from tBuOOH-induced cytotoxicity. Furthermore, ASSNAC increases the level of mice spinal cord and brain glutathione (by 54% and 47%, respectively) and attenuates the clinical symptoms of experimental autoimmune encephalomyelitis (EAE) in mice. In conclusion, these data implicate ASSNAC to protect nerve cells, both in vitro and in vivo, from oxidative stress and thereby to attenuate the clinical symptoms of EAE, suggesting its potential use for the treatment of neurodegenerative diseases.
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Authors | Naphtali Savion, Nira Izigov, Milana Morein, Sarah Pri-Chen, Shlomo Kotev-Emeth |
Journal | Neuroscience letters
(Neurosci Lett)
Vol. 583
Pg. 108-13
(Nov 07 2014)
ISSN: 1872-7972 [Electronic] Ireland |
PMID | 25263785
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- Allyl Compounds
- Neuroprotective Agents
- S-allylmercapto-N-acetylcysteine
- Acetylcysteine
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Topics |
- Acetylcysteine
(analogs & derivatives, pharmacology, therapeutic use)
- Allyl Compounds
(pharmacology, therapeutic use)
- Animals
- Cell Line, Tumor
- Encephalomyelitis, Autoimmune, Experimental
(drug therapy, metabolism)
- Female
- Humans
- Mice, Inbred C57BL
- Neurons
(drug effects, metabolism)
- Neuroprotective Agents
(pharmacology, therapeutic use)
- Oxidative Stress
(drug effects)
- Rats
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