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

岩藻黄素对β-淀粉样蛋白致细胞损伤的神经保护作用（英文）

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 the β-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 theraoeutic agent for AD.

阿尔茨海默病(Alzheimer’s disease,AD)是老年人常见认知障碍疾病之一。岩藻黄素是从可以食用海藻中发现的一种类红萝卜素,它是海藻类发挥抗癌、抗氧化以及抗炎症等生物活性的主要活性物质。本文在原代培养的大脑皮质神经元和PC12细胞上观察了岩藻黄素对Aβ所致神经毒性的保护作用。通过细胞活力测定,Hoechst33342和碘化丙啶(PI)双染评价了岩藻黄素对Aβ所致神经毒性的保护作用。通过检测总抗氧化能力(T-AOC),脂质过氧化产物丙二醛(MDA)水平和超氧化物歧化酶(SOD)的活力评价了该药物的抗氧化作用。结果显示,Aβ会导致原代培养的大脑皮质神经元和PC12细胞的死亡。岩藻黄素预处理,可以降低Aβ所致的细胞死亡。T-AOC、MDA和SOD的检测结果显示,Aβ作用后可以导致T-AOC和SOD活力的降低和MDA含量的升高。给予岩藻黄素预处理后,T-AOC、SOD和MDA的检测结果显示出了相反的趋势。这提示岩藻黄素预处理可以增加神经元抗氧化能力和降低脂质过氧化水平。以上结果表明,岩藻黄素可以通过降低氧化应激来预防Aβ所致的神经毒性,可能是预防或治疗AD的潜在药物。