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DOI 10.3390/ijms22137225

Медицинская библиотека · International journal of molecular sciences · 2021

EVOO Polyphenols Relieve Synergistically Autophagy Dysregulation in a Cellular Model of Alzheimer's Disease.

Leri Manuela, Bertolini Andrea, Stefani Massimo, Bucciantini Monica

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Аннотация

(1)

Background

Autophagy, the major cytoplasmic process of substrate turnover, declines with age, contributing to proteostasis decline, accumulation of harmful protein aggregates, damaged mitochondria and to ROS production. Accordingly, abnormalities in the autophagic flux may contribute to many different pathophysiological conditions associated with ageing, including neurodegeneration. Recent data have shown that extra-virgin olive oil (EVOO) polyphenols stimulate cell defenses against plaque-induced neurodegeneration, mainly, through autophagy induction. (2)

Methods

We carried out a set of in vitro experiments on SH-SY5Y human neuroblastoma cells exposed to toxic Aβ1-42 oligomers to investigate the molecular mechanisms involved in autophagy activation by two olive oil polyphenols, oleuropein aglycone (OleA), arising from the hydrolysis of oleuropein (Ole), the main polyphenol found in olive leaves and drupes and its main metabolite, hydroxytyrosol (HT). (3)

Results

Our data show that the mixture of the two polyphenols activates synergistically the autophagic flux preventing cell damage by Aβ1-42 oligomers., in terms of ROS production, and impairment of mitochondria. (4)

Conclusion

Our results support the idea that EVOO polyphenols act synergistically in autophagy modulation against neurodegeneration. These data confirm and provide the rationale to consider these molecules, alone or in combination, as promising candidates to contrast ageing-associated neurodegeneration.

Для цитирования: Leri Manuela, Bertolini Andrea, Stefani Massimo, Bucciantini Monica. EVOO Polyphenols Relieve Synergistically Autophagy Dysregulation in a Cellular Model of Alzheimer's Disease.. International journal of molecular sciences. 2021. DOI: 10.3390/ijms22137225.

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