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Innovative anthocyanin/anthocyanidin formulation protects SK-N-SH cells against the amyloid-β peptide-induced toxicity: Relevance to alzheimer’s disease

Belkacemi, Abdenour; Ramassamy, Charles (2015). Innovative anthocyanin/anthocyanidin formulation protects SK-N-SH cells against the amyloid-β peptide-induced toxicity: Relevance to alzheimer’s disease Central Nervous System Agents in Medicinal Chemistry , vol. 16 , nº 1. p. 37-49. DOI: 10.2174/1871524915666150730125532.

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Résumé

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder of aging. It is a multifactorial disease with several overlapping pathways. Therefore, successful therapy should target several pathological features simultaneously. In this regard, cumulative data have demonstrated that polyphenols can display neuroprotective effects through different mechanisms. In this study, we tested the hypothesis that a mixture of anthocyanins/anthocyanidins presents in the formulation MAF14001 may mitigate the amyloid-β peptide (Aβ) toxicity. Anthocyanins are a class of polyphenols capable to cross the blood brain barrier and their intake is associated to a reduced risk of some several chronic diseases. Our results showed that the formulation MAF14001 can protect SK-N-SH cells against Aβ-induced toxicity. From 5 μM, MAF14001 protected SK-N-SH cells against Aβ toxicity by preventing oxidative stress, mitochondrial dysfunction and apoptosis. Furthermore, MAF14001 might directly interact with Aβ to prevent its aggregation process, a key process on Aβ-induced oxidative stress. Indeed, in the presence of MAF14001, Aβ was less susceptible to fibrillation. Finally, MAF14001 decreased the tau phosphorylation (Ser-202) induced by Aβ. Altogether, these results demonstrated that MAF14001 could target multiple mechanisms involved in the etiology of AD and could be useful in preventing and treating AD.

Type de document: Article
Mots-clés libres: Amyloid-beta; Apoptosis; Mitochondrial membrane potential; Oxidative stress; Polyphenols; Protein carbonyls; Tau phosphorylation; amyloid beta protein; anthocyanin; proanthocyanidin; thioflavine; Alzheimer disease; Article; cell death; cell structure; cell survival; cell viability; circular dichroism; collagen fibril; controlled study; cytotoxicity; human; human cell; immunocytochemistry; neuroblastoma cell line; protein analysis; protein carbonylation; protein expression; protein phosphorylation transmission electron microscopy; ultraviolet spectrophotometry; Western blotting
Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 12 oct. 2017 13:54
Dernière modification: 12 oct. 2017 13:54
URI: http://espace.inrs.ca/id/eprint/4593

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