title: Innovative anthocyanins formulation protects neuronal-like cells against oxidative stress-induced damage: Pharmacotherapeutic application for Alzheimer's disease.
abstract: Oxidative stress is involved in the etiology of multiple chronic diseases including Parkinson's and Alzheimer's diseases (AD). Moreover, it is believed to be a primary cause in diseases pathogenesis. For instance, in AD lipid peroxidation by-products such as acrolein accumulated specifically in vulnerable regions of the brain from mild cognitive impairment and preclinical AD patients. Acrolein is a highly reactive aldehyde seen also as an initiator of oxidative stress. Although severalstudies have demonstrated that polyphenol-rich extracts could exert beneficial effect on cognitive impairment and oxidative stress, only a few of them could reach the brain. Among them, anthocyanins have been detected in hippocampus but in a very small amount. Thus, we hypothesised that polyphenols could have synergic effect at low concentrations leading to the neuroprotective effect. Our screening experiments lead to a formulation containing a mix of different anthocyanins (MAF) with antioxidant and neuroprotective effect at very low doses. Our results demonstrated that MAF showed a protective effect against acrolein- and b-amyloid-induced SK-N-SH cell toxicity. Our data demonstrated that MAF was able to lower protein carbonyl levels induced by acrolein or ß-amyloid. Moreover, MAF prevented glutathione depletion induced by acrolein. Our results also showed that MAF prevented the expression of ?-glutamylcystein synthetase, the nuclear translocation of Nrf2, the activation of both NF-?B and p66HSC by acrolein. In conclusion, we demonstrated that the innovative anthocyanin formulationMAF was not only a powerful antioxidant, but could also regulate cellular pathways involved in antioxidant defenses and cell survival. These effects of MAF were observed with low concentrations suggesting a synergistic effect of these polyphenolic compounds. These results indicate that MAF could be a promising agent for AD prevention.
authors.affiliation: Institut National de la Recherche Scientifique-Institut Armand-Frappier. Laval, Quebec, Canada.
authors.forename: Belkacemi
authors.initials: B
authors.lastname: Abdenour
authors.affiliation: Institut National de la Recherche Scientifique-Institut Armand-Frappier. Laval, Quebec, Canada. Electronic address: charles.ramassamy@iaf.inrs.ca.
authors.forename: Ramassamy
authors.initials: R
authors.lastname: Charles