Fucoidan inhibits amyloid-beta-induced toxicity in transgenic caenorhabditis elegans by reducing the accumulation of amyloid-beta and decreasing reactive oxygen species.
Fucoidan inhibits amyloid-beta-induced toxicity in transgenic caenorhabditis elegans by reducing the accumulation of amyloid-beta and decreasing reactive oxygen species.
复制标题
褐藻糖胶通过减少β淀粉样蛋白的积累和减少活性氧来抑制转基因秀丽隐杆线虫中β淀粉样蛋白诱导的毒性。
DOI：
10.1039/c7fo00662d
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发表时间：
2017
期刊：
影响因子：
6.1
通讯作者：
Yan Zhao
中科院分区：
文献类型：
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作者：
Xuelian Wang;kaixuan Yi;Yan Zhao
阿尔茨海默病（Alzheimer's disease，AD）是最常见的与年龄相关的神经退行性疾病。随着人口老龄化的加剧，AD正成为老年人残疾和死亡的主要原因之一。然而，目前还没有治愈这种疾病的方法。褐藻糖胶是一种复杂的硫酸多糖，主要存在于褐藻中。最近的研究表明，岩藻依聚糖具有神经保护作用，并可能用于治疗和/或预防神经退行性疾病，如AD。本研究以转基因秀丽隐杆线虫（C. habditis elegans）为模型，研究了褐藻糖胶对Abeta诱导的细胞毒性的影响及其可能机制。elegans）AD模型。结果表明，岩藻多糖的补充减轻了由Abeta诱导的麻痹表型。岩藻依聚糖处理减少了AD动物中Abeta沉积物的数量。对Abeta水平的进一步分析表明，岩藻依聚糖显著降低了转基因AD C中Abeta的积累。优雅结果发现，岩藻依聚糖处理提高了蛋白体的活性;因此，岩藻依聚糖可能通过促进蛋白水解来减少Abeta积累。此外，岩藻依聚糖处理减少了由Abeta诱导刺激的活性氧（ROS）的产生。这些结果表明，褐藻糖胶可能对转基因AD C细胞的毒性具有保护作用。通过减少毒性Abeta的积累和减少Abeta诱导的ROS的产生，从而改善AD表型的进展。
Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. As the aging population is increasing, AD is becoming one of the leading causes of disability and death among the elderly. However, currently there is no cure for this disease. Fucoidan is a complex sulfated polysaccharide mainly found in brown seaweed. Recent studies have shown that fucoidan is neuroprotective and may have potential to be used for treating and/or preventing neurodegenerative diseases such as AD. In this study, we investigated the effects and possible mechanisms of fucoidan on Abeta induced toxicity in a transgenic Caenorhabditis elegans (C. elegans) AD model. The results showed that the supplementation of fucoidan alleviated the paralyzed phenotype induced by Abeta. The number of Abeta deposits in the AD animals was reduced by fucoidan treatment. Further analysis of the levels of Abeta showed that fucoidan significantly decreased the accumulation of Abeta in transgenic AD C. elegans. It was found that fucoidan treatment elevated the activity of proteosomes; therefore, fucoidan might decrease Abeta accumulation by promoting proteolysis. In addition, fucoidan treatment reduced the production of reactive oxygen species (ROS) stimulated by Abeta induction. These results suggested that fucoidan might exert its protective effects against Abeta-induced toxicity in transgenic AD C. elegans by reducing the accumulation of toxic Abeta and decreasing Abeta-induced production of ROS, thus ameliorating the progression of the AD phenotype.