NDLI: Innovative anthocyanins formulation protects neuronal-like cells against oxidative stress-induced damage: Pharmacotherapeutic application for Alzheimer's disease.

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Innovative anthocyanins formulation protects neuronal-like cells against oxidative stress-induced damage: Pharmacotherapeutic application for Alzheimer's disease.

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Innovative anthocyanins formulation protects neuronal-like cells against oxidative stress-induced damage: Pharmacotherapeutic application for Alzheimer's disease.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Abdenour, Belkacemi Charles, Ramassamy
Description	Country affiliation: Canada Author Affiliation: Abdenour B ( Institut National de la Recherche Scientifique-Institut Armand-Frappier. Laval, Quebec, Canada.); Charles R ( Institut National de la Recherche Scientifique-Institut Armand-Frappier. Laval, Quebec, Canada. Electronic address: charles.ramassamy@iaf.inrs.ca.)
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.
File Format	HTM / HTML
ISSN	08915849
Issue Number	Suppl 1
Journal	Free Radical Biology and Medicine
Volume Number	75
e-ISSN	18734596
Language	English
Publisher	Elsevier
Publisher Date	2014-10-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Biochemistry

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