Effects of the Aphanizomenon flos-aquae Extract (Klamin®) on a Neurodegeneration Cellular Model.
D NuzzoG PrestiP PiconeG GalizziE GulottaS GiulianoC ManninoV GambinoS ScoglioMarta Di CarloPublished in: Oxidative medicine and cellular longevity (2018)
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.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- anti inflammatory
- dna damage
- ischemia reperfusion injury
- high throughput
- cell death
- high resolution
- cell proliferation
- big data
- mass spectrometry
- heat shock
- machine learning
- cell cycle arrest
- endoplasmic reticulum stress
- nuclear factor
- blood brain barrier
- subarachnoid hemorrhage
- aqueous solution
- brain injury
- heat stress
- monoclonal antibody