Department of Biomedical, Experimental and Clinical Sciences, University of Firenze, 50134 Firenze, Italy.
Department of Surgical, Medical, Molecular Pathology and Critical Care Medicine, University of Pisa, 56126 Pisa, Italy.
Int J Mol Sci. 2021 Jul 5;22(13):7225. doi: 10.3390/ijms22137225.
(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 Aβ 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 Aβ 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.
(1) 背景：自噬是细胞内物质代谢的主要过程，随着年龄的增长而下降，导致蛋白质稳态下降、有害蛋白质聚集体积累、受损线粒体和 ROS 产生。因此，自噬通量的异常可能导致与衰老相关的许多不同的病理生理状况，包括神经退行性变。最近的数据表明，特级初榨橄榄油（EVOO）多酚通过诱导自噬来刺激细胞防御斑块诱导的神经退行性变。
(2) 方法：我们对暴露于有毒 Aβ 低聚物的 SH-SY5Y 人神经母细胞瘤细胞进行了一系列体外实验，以研究两种橄榄油多酚——橄榄苦苷苷元（OleA）和羟基酪醇（HT），从橄榄叶和核果中发现的主要多酚橄榄苦苷水解而来，对自噬激活的分子机制。
(3) 结果：我们的数据表明，两种多酚的混合物通过激活自噬通量，协同地防止 Aβ 低聚物引起的细胞损伤，在 ROS 产生和线粒体损伤方面。
(4) 结论：我们的结果支持了 EVOO 多酚通过协同作用调节自噬来对抗神经退行性变的观点。这些数据证实并为考虑这些分子（单独或联合）作为对抗与衰老相关的神经退行性变的有前途的候选物提供了依据。
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