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Antioxidative and Anti-Inflammatory Neuroprotective Effects of Astaxanthin and Canthaxanthin in Nerve Growth Factor Differentiated PC12 Cells

Authors

  • Kung-chi Chan,

    1. Author Chan is with Dept. of Food and Nutrition, Providence Univ., Taichung County, Taiwan. Author Mong is with Dept. of Health and Nutrition Biotechnology, Asia Univ., Taichung County, Taiwan. Author Yin is with Dept. of Nutrition, China Medical Univ., Taichung City, Taiwan. Direct inquiries to author Yin (E-mail: mcyin@mail.cmu.edu.tw).
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  • Mei-chin Mong,

    1. Author Chan is with Dept. of Food and Nutrition, Providence Univ., Taichung County, Taiwan. Author Mong is with Dept. of Health and Nutrition Biotechnology, Asia Univ., Taichung County, Taiwan. Author Yin is with Dept. of Nutrition, China Medical Univ., Taichung City, Taiwan. Direct inquiries to author Yin (E-mail: mcyin@mail.cmu.edu.tw).
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  • Mei-chin Yin

    1. Author Chan is with Dept. of Food and Nutrition, Providence Univ., Taichung County, Taiwan. Author Mong is with Dept. of Health and Nutrition Biotechnology, Asia Univ., Taichung County, Taiwan. Author Yin is with Dept. of Nutrition, China Medical Univ., Taichung City, Taiwan. Direct inquiries to author Yin (E-mail: mcyin@mail.cmu.edu.tw).
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Abstract

ABSTRACT:  Nerve growth factor differentiated PC12 cells were used to examine the antioxidative and anti-inflammatory effects of astaxanthin (AX) and canthaxanthin (CX). PC12 cells were pretreated with AX or CX at 10 or 20 μM, and followed by exposure of hydrogen peroxide (H2O2) or 1-methyl-4-phenylpyridinium ion (MPP+) to induce cell injury. H2O2 or MPP+ treatment significantly decreased cell viability, increased lactate dehydrogenase (LDH) release, enhanced DNA fragmentation, and lowered mitochondrial membrane potential (MMP) (P < 0.05). The pretreatments from AX or CX concentration-dependently alleviated H2O2 or MPP+-induced cell death, LDH release, DNA fragmentation, and MMP reduction (P < 0.05). Either H2O2 or MPP+ treatment significantly increased malonyldialdehyde (MDA) and reactive oxygen species (ROS) formations, decreased glutathione content, and lowered glutathione peroxidase (GPX) and catalase activities (P < 0.05). The pretreatments from AX or CX significantly retained GPX and catalase activities, and decreased MDA and ROS formations (P < 0.05). H2O2 or MPP+ treatment significantly decreased Na+-K+-ATPase activity, elevated caspase-3 activity and levels of interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α (P < 0.05); and the pretreatments from these agents significantly restored Na+-K+-ATPase activity, suppressed caspase-3 activity and release of IL-1, IL-6, and TNF-α (P < 0.05). Based on the observed antioxidative and anti-inflammatory protection from AX and CX, these 2 compounds were potent agents against neurodegenerative disorder.

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