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Effects of the Aphanizomenon flos-aquae Extract (Klamin®) on a Neurodegeneration Cellular Model

机译:大花紫苏提取物(Klamin®)对神经退行性细胞模型的影响

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摘要

Cyanobacteria have been recognized as a source of bioactive molecules to be employed in nutraceuticals, pharmaceuticals, and functional foods. An extract of Aphanizomenon flos-aquae (AFA), commercialized as Klamin®, was subjected to chemical analysis to determine its compounds. The AFA extract Klamin® resulted to be nontoxic, also at high doses, when administered onto LAN5 neuronal cells. Its scavenging properties against ROS generation were evaluated by using DCFH-DA assay, and its mitochondrial protective role was determined by JC-1 and MitoSOX assays. Klamin® exerts a protective role against beta amyloid- (Aβ-) induced toxicity and against oxidative stress. Anti-inflammatory properties were demonstrated by NFβB nuclear localization and activation of IL-6 and IL-1β inflammatory cytokines through ELISA. Finally, by using thioflavin T (ThT) and fluorimetric measures, we found that Klamin® interferes with Aβ aggregation kinetics, supporting the formation of smaller and nontoxic structures compared to toxic Aβ aggregates alone. Altogether, these data indicate that the AFA extract may play a protective role against mechanisms leading to neurodegeneration.
机译:蓝细菌已被认为是在营养保健品,药物和功能性食品中使用的生物活性分子的来源。商业化的Aphanizomenon flos-aquae(AFA)提取物经过化学分析,以确定其化合物。当将AFA提取物施用于LAN5神经元细胞时,即使在高剂量下也无毒。使用DCFH-DA分析评估其对ROS产生的清除性能,并通过JC-1和MitoSOX分析确定其对线粒体的保护作用。 Klamin®对β淀粉样蛋白(Aβ-)诱导的毒性和氧化应激起保护作用。通过NFβB核定位和IL-6和IL-1β炎性细胞因子的激活证明了抗炎特性。最后,通过使用硫代黄素T(ThT)和荧光法,我们发现Klamin®会干扰Aβ聚集动力学,与单独的有毒Aβ聚集体相比,支持形成较小的无毒结构。总而言之,这些数据表明AFA提取物可能对导致神经变性的机制起保护作用。

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