Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2018, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2018/2856063
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Funding
- CIBERNED
- Ministerio de Economia y Competitividad [SAF2016-75292-R]
- Gobierno Vasco
- Ikerbasque, Basque Foundation for Science
- UPV/EHU
- Swedish Research Council (VR) International postdoctoral grant DNR [637-2013-503]
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Amyloid beta- (A beta-) mediated ROS overproduction disrupts intraneuronal redox balance and exacerbates mitochondrial dysfunction which leads to neuronal injury. Polyphenols have been investigated as therapeutic agents that promote neuroprotective effects in experimental models of brain injury and neurodegenerative diseases. The aim of this study was to identify the neuroprotective effects of morin and mangiferin against A beta oligomers in cultured cortical neurons and organotypic slices as well as their mechanisms of action. Cell death caused by A beta oligomers in neuronal cultures was decreased in the presence of micromolar concentrations of mangiferin or morin, which in turn attenuated oxidative stress. The neuroprotective effects of antioxidants against A beta were associated with the reduction of A beta-induced calcium load to mitochondria; mitochondrial membrane depolarization; and release of cytochrome c from mitochondria, a key trigger of apoptosis. Additionally, we observed that both polyphenols activated the endogenous enzymatic antioxidant system and restored oxidized protein levels. Finally, A beta induced an impairment of energy homeostasis due to a decreased respiratory capacity that was mitigated by morin and mangiferin. Overall, the beneficial effects of polyphenols in preventing mitochondrial dysfunction and neuronal injury in AD cell models suggest that morin and mangiferin hold promise for the treatment of this neurological disorder.
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