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
Affiliations
Chi-Huang Chang
Department of Biotechnology, College of Medical and Health Care, Hungkuang University, No. 1018, Sec. 6, Taiwan Boulevard, Shalu District, Taichung City 43302, Taiwan
Kuan-Chou Chen
Department of Urology, School of Medicine, College of Medicine, Taipei Medical University, 250 Wu-Shing St., Taipei 11031, Taiwan
Kuo-Chun Liaw
Department of Biotechnology, College of Medical and Health Care, Hungkuang University, No. 1018, Sec. 6, Taiwan Boulevard, Shalu District, Taichung City 43302, Taiwan
Chiung-Chi Peng
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 11031, Taiwan
Robert Y. Peng
Department of Biotechnology, College of Medical and Health Care, Hungkuang University, No. 1018, Sec. 6, Taiwan Boulevard, Shalu District, Taichung City 43302, Taiwan
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.
