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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。
Alzheimer’s disease (AD) is one of the common cognitive disorders in the elderly. Fucoxanthin, a carotenoid found in edible seaweeds, is a major active substance of seaweed that exerts its biological activities such as anti-cancer, antioxidant and anti-inflammatory properties. In this paper, primary cultured cerebral cortical neurons and PC12 cells were observed fuguantin Aβ-induced neurotoxicity. The protective effect of fucoxanthin against Aβ-induced neurotoxicity was evaluated by cell viability assay, double staining with Hoechst 33342 and propidium iodide (PI). The antioxidant activity of the drug was evaluated by detecting total antioxidant capacity (T-AOC), malondialdehyde (MDA) level and superoxide dismutase (SOD) activity. The results showed that Aβ resulted in the death of primary cultured cerebral cortical neurons and PC12 cells. Preconditioning with fucoxanthin reduced Aβ-induced cell death. The results of T-AOC, MDA and SOD showed that Aβ could decrease the activity of T-AOC and SOD and increase the content of MDA. After pretreatment with fucoxanthin, the T-AOC, SOD and MDA test results showed the opposite trend. This suggests that fucoxanthin preconditioning increases neuronal antioxidant capacity and decreases lipid peroxidation. The above results show that fucoxanthin can prevent Aβ-induced neurotoxicity by reducing oxidative stress and may be a potential drug for the prevention or treatment of AD.