岩藻多糖对Aβ25-35诱导神经元凋亡和突起萎缩的抑制作用

Protective Effect of Fucoidan on Aβ25-35-induced Neuronal Injury and Neurite Atrophy

【目的】研究海带岩藻多糖(Fucoidan)对Aβ25-35(Amyloidβ)诱导原代皮层神经突起萎缩和神经元凋亡的抑制作用。【方法】以Aβ25-35诱导的人神经母细胞瘤细胞(SH-SY5Y)和原代小鼠皮层神经元损伤为模型,采用CCK8法测定细胞存活率,免疫细胞化学法测定岩藻多糖对神经突起再生和神经元的保护作用。【结果】CCK8结果表明,岩藻多糖在0.1~1000μg/mL时对SH-SY5Y细胞无明显毒性作用(P>0.05),在10~1000μg/mL时可显著降低Aβ25-35诱导的SH-SY5Y细胞凋亡(P<0.05),且呈现浓度依赖性;对该结果在原代小鼠皮层神经元上进行验证,发现岩藻多糖在0.1~1.0 mg/mL浓度时显著降低Aβ25-35诱导的神经元凋亡(P<0.01),同时极显著抑制Aβ25-35造成的神经突起萎缩并促进突起再伸长(P<0.001)。【结论】海带岩藻多糖可显著抑制Aβ25-35诱导的神经突起萎缩和神经元凋亡,促进突起再生,提示其可作为阿尔茨海默病药物开发的先导化合物。

【Objective】To investigate the effect of Fucoidan on Aβ25-35-induced neuronal injury and neurite atrophy.【Methods】Aβ25-35-induced SH-SY5Y and primary mouse cortical neuronal injury were constructed as Alzheimer’s disease(AD)models.The cell viability was carried out by CCK8 method,and the protective effects of Fucoidan on neurons and neurite outgrowth were determined by immunocytochemistry.【Results】The CCK8 test indicated that fucoidan has no toxic effect on SH-SY5Y cells at concentrations from 0.1 to 1000μg/mL(P>0.05).It could significantly reduce Aβ25-35-induced neuronal apoptosis of SH-SY5Y cells(P<0.05).This finding has been validated using primary cortical neurons culture.Fucoidan at 0.1―1.0 mg/mL significantly reduces Aβ25-35-induced neuronal apoptosis and neurite atrophy,and promote neurite outgrowth.【Conclusions】Fucoidan significantly inhibits Aβ25-35-induced neurite atrophy and neuronal apoptosis and promotes neurite regrowth,and it might be a potential leading molecule for the treatment of AD.