Astaxanthin protects PC12 cells against homocysteine- And glutamate-induced neurotoxicity

Chi Huang Chang; Kuan Chou Chen; Kuo Chun Liaw; Chiung Chi Peng; Robert Y. Peng

doi:10.3390/molecules25010214

Astaxanthin protects PC12 cells against homocysteine- And glutamate-induced neurotoxicity

Chi Huang Chang, Kuan Chou Chen, Kuo Chun Liaw, Chiung Chi Peng, Robert Y. Peng

Research output: Contribution to journal › Article › peer-review

21 Citations (Scopus)

Abstract

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 EC₅₀ 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.

Original language	English
Article number	214
Journal	Molecules
Volume	25
Issue number	1
DOIs	https://doi.org/10.3390/molecules25010214
Publication status	Published - Jan 5 2020

Keywords

Astaxanthin (ATX)
Glutamate (Glu)
Homocysteine (Hcy)
Intrinsic apoptotic pathways
Neuroprotective
PC12 cells

ASJC Scopus subject areas

Analytical Chemistry
Chemistry (miscellaneous)
Molecular Medicine
Pharmaceutical Science
Drug Discovery
Physical and Theoretical Chemistry
Organic Chemistry

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10.3390/molecules25010214

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title = "Astaxanthin protects PC12 cells against homocysteine- And glutamate-induced neurotoxicity",

abstract = "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 EC50 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.",

keywords = "Astaxanthin (ATX), Glutamate (Glu), Homocysteine (Hcy), Intrinsic apoptotic pathways, Neuroprotective, PC12 cells",

author = "Chang, {Chi Huang} and Chen, {Kuan Chou} and Liaw, {Kuo Chun} and Peng, {Chiung Chi} and Peng, {Robert Y.}",

note = "Publisher Copyright: {\textcopyright} 2020 by the authors.",

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doi = "10.3390/molecules25010214",

language = "English",

volume = "25",

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AU - Chang, Chi Huang

AU - Chen, Kuan Chou

AU - Liaw, Kuo Chun

AU - Peng, Chiung Chi

AU - Peng, Robert Y.

PY - 2020/1/5

Y1 - 2020/1/5

N2 - 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 EC50 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.

AB - 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 EC50 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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KW - Glutamate (Glu)

KW - Homocysteine (Hcy)

KW - Intrinsic apoptotic pathways

KW - Neuroprotective

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Astaxanthin protects PC12 cells against homocysteine- And glutamate-induced neurotoxicity

Abstract

Keywords

ASJC Scopus subject areas

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