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Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity

Memory impairment has been shown to be associated with glutamate (Glu) excitotoxicity, homocysteine (Hcy) accumulation, and oxidative stress. We hypothesize that Glu and Hcy could damage neuronal cells, while astaxanthin (ATX) could be beneficial to alleviate the adverse effects. Using PC12 cell mod...

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Detalles Bibliográficos
Autores principales: Chang, Chi-Huang, Chen, Kuan-Chou, Liaw, Kuo-Chun, Peng, Chiung-Chi, Peng, Robert Y.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6982875/
https://www.ncbi.nlm.nih.gov/pubmed/31948056
http://dx.doi.org/10.3390/molecules25010214
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author Chang, Chi-Huang
Chen, Kuan-Chou
Liaw, Kuo-Chun
Peng, Chiung-Chi
Peng, Robert Y.
author_facet Chang, Chi-Huang
Chen, Kuan-Chou
Liaw, Kuo-Chun
Peng, Chiung-Chi
Peng, Robert Y.
author_sort Chang, Chi-Huang
collection PubMed
description Memory impairment has been shown to be associated with glutamate (Glu) excitotoxicity, homocysteine (Hcy) accumulation, and oxidative stress. We hypothesize that Glu and Hcy could damage neuronal cells, while astaxanthin (ATX) could be beneficial to alleviate the adverse effects. Using PC12 cell model, we showed that Glu and Hcy provoked a huge amount of reactive oxygen species (ROS) production, causing mitochondrial damage at EC(50) 20 and 10 mm, respectively. The mechanisms of action include: (1) increasing calcium influx; (2) producing ROS; (3) initiating lipid peroxidation; (4) causing imbalance of the Bcl-2/Bax homeostasis; and (5) activating cascade of caspases involving caspases 12 and 3. Conclusively, the damages caused by Glu and Hcy to PC12 cells can be alleviated by the potent antioxidant ATX.
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spelling pubmed-69828752020-02-06 Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity Chang, Chi-Huang Chen, Kuan-Chou Liaw, Kuo-Chun Peng, Chiung-Chi Peng, Robert Y. Molecules Article Memory impairment has been shown to be associated with glutamate (Glu) excitotoxicity, homocysteine (Hcy) accumulation, and oxidative stress. We hypothesize that Glu and Hcy could damage neuronal cells, while astaxanthin (ATX) could be beneficial to alleviate the adverse effects. Using PC12 cell model, we showed that Glu and Hcy provoked a huge amount of reactive oxygen species (ROS) production, causing mitochondrial damage at EC(50) 20 and 10 mm, respectively. The mechanisms of action include: (1) increasing calcium influx; (2) producing ROS; (3) initiating lipid peroxidation; (4) causing imbalance of the Bcl-2/Bax homeostasis; and (5) activating cascade of caspases involving caspases 12 and 3. Conclusively, the damages caused by Glu and Hcy to PC12 cells can be alleviated by the potent antioxidant ATX. MDPI 2020-01-05 /pmc/articles/PMC6982875/ /pubmed/31948056 http://dx.doi.org/10.3390/molecules25010214 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Chang, Chi-Huang
Chen, Kuan-Chou
Liaw, Kuo-Chun
Peng, Chiung-Chi
Peng, Robert Y.
Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity
title Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity
title_full Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity
title_fullStr Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity
title_full_unstemmed Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity
title_short Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity
title_sort astaxanthin protects pc12 cells against homocysteine- and glutamate-induced neurotoxicity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6982875/
https://www.ncbi.nlm.nih.gov/pubmed/31948056
http://dx.doi.org/10.3390/molecules25010214
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