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

Abstract

Cyanobacteria have been recognized as a source of bioactive molecules to be employed in nutraceuticals, pharmaceuticals, and functional foods. An extract of <i>Aphanizomenon flos-aquae</i> (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- (A<i>β-</i>) induced toxicity and against oxidative stress. Anti-inflammatory properties were demonstrated by NF<i>β</i>B nuclear localization and activation of IL-6 and IL-1<i>β</i> inflammatory cytokines through ELISA. Finally, by using thioflavin T (ThT) and fluorimetric measures, we found that Klamin® interferes with A<i>β</i> aggregation kinetics, supporting the formation of smaller and nontoxic structures compared to toxic A<i>β</i> aggregates alone. Altogether, these data indicate that the AFA extract may play a protective role against mechanisms leading to neurodegeneration.