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Journal of Chinese Pharmaceutical Sciences ›› 2015, Vol. 24 ›› Issue (7): 467-474.DOI: 10.5246/jcps.2015.07.060

• Original articles • Previous Articles     Next Articles

Neuroprotective effect of fucoxanthin on β-amyloid-induced cell death

Xin Zhao1, Shiping Zhang1, Chunna An1, Hongning Zhang2, Yi Sun1, Yanmei Li2, Xiaoping Pu1*   

  1. 1. Department of Molecular and Cellular Pharmacology, State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University Health Science Center, , Beijing 100191, China
    2. Beijing Gingko Group Biological Technology Co., Ltd., Beijing 100044, China
  • Received:2014-12-26 Revised:2015-02-26 Online:2015-07-28 Published:2015-03-27
  • Contact: Tel./Fax: 86-10-82802431
  • Supported by:

    National Natural Science Foundation of China (Grant No. 81202937), the National Key Scientific Instrument and Equipment Development Project (Grant No. 2013YQ030651) and the New Teachers’ Fund from School of Pharmaceutical Sciences, Peking University (Grant No. BMU20100090).

Abstract:

Alzheimer’s disease (AD) is one of the most common cognitive disorders of the elderly. Fucoxanthin is a carotenoid that is found in common edible seaweed, and it is considered as a major active compound of marine algae with cancer-preventing,antioxidant and anti-inflammatory properties. In this study, we investigated the ability of fucoxanthin to protect against theβ-amyloid protein (Aβ)-induced neurotoxicity in primary cortical cultured neurons and PC12 cells. Neuroprotective effects of fucoxanthin were determined by measuring cell viability and nuclei double-staining with Hoechst 33342 and propidium iodide following Aβ treatment with or without fucoxanthin. Moreover, we also evaluated its potential mechanism on antioxidation by detecting the total antioxidant capacity (T-AOC), level of lipid peroxidation malondialdehyde (MDA) and activity of superoxide dismutase (SOD). We found that exposure of cortical cultured neurons or PC12 cells to Aβ resulted in neuronal cell death, whereas pre-treatment with fucoxanthin reduced Aβ-induced cell death. The data on the T-AOC, MDA level and SOD activity showed that Aβ treatment resulted in decreases in T-AOC and SOD activity and an increase in MDA level. After fucoxanthin administration, the results of T-AOC, MDA level and SOD activity showed an opposite trend, indicating that T-AOC was increased and MDA level was reduced. These results suggested that fucoxanthin prevented Aβ-induced neurotoxicity through attenuating oxidative stress induced by Aβ. Therefore, fucoxanthin might be useful as a potential preventive or therapeutic agent for AD.

Key words: Alzheimer’s disease, Neurodegenerative disorder, Antioxidation

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