S-Allylmercapto-N-acetylcysteine (ASSNAC) protects cultured nerve cells from oxidative stress and attenuates experimental autoimmune encephalomyelitis
| Autor: | Sarah Pri-Chen, Shlomo Kotev-Emeth, Nira Izigov, Milana Morein, Naphtali Savion |
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| Rok vydání: | 2014 |
| Předmět: |
Encephalomyelitis
Autoimmune Experimental Pharmacology Biology medicine.disease_cause chemistry.chemical_compound In vivo Cell Line Tumor medicine Animals Humans Cytotoxicity Neurons General Neuroscience Experimental autoimmune encephalomyelitis Glutathione medicine.disease Spinal cord In vitro Acetylcysteine Rats Allyl Compounds Mice Inbred C57BL Oxidative Stress Neuroprotective Agents medicine.anatomical_structure chemistry Cell culture Immunology Female Oxidative stress |
| Zdroj: | Neuroscience Letters. 583:108-113 |
| ISSN: | 0304-3940 |
| DOI: | 10.1016/j.neulet.2014.09.034 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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