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多酚、自噬和神经退行性疾病:综述。

Polyphenols, Autophagy and Neurodegenerative Diseases: A Review.

机构信息

Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Mysuru 570015, India.

Center for Experimental Pharmacology and Toxicology, Central Animal Facility, JSS Academy of Higher Education and Research, Mysuru 570015, India.

出版信息

Biomolecules. 2023 Jul 31;13(8):1196. doi: 10.3390/biom13081196.

DOI:10.3390/biom13081196
PMID:37627261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10452370/
Abstract

Polyphenols are secondary metabolites from plant origin and are shown to possess a wide range of therapeutic benefits. They are also reported as regulators of autophagy, inflammation and neurodegeneration. The autophagy pathway is vital in degrading outdated organelles, proteins and other cellular wastes. The dysregulation of autophagy causes proteinopathies, mitochondrial dysfunction and neuroinflammation thereby contributing to neurodegeneration. Evidence reveals that polyphenols improve autophagy by clearing misfolded proteins in the neurons, suppress neuroinflammation and oxidative stress and also protect from neurodegeneration. This review is an attempt to summarize the mechanism of action of polyphenols in modulating autophagy and their involvement in pathways such as mTOR, AMPK, SIRT-1 and ERK. It is evident that polyphenols cause an increase in the levels of autophagic proteins such as beclin-1, microtubule-associated protein light chain (LC3 I and II), sirtuin 1 (SIRT1), etc. Although it is apparent that polyphenols regulate autophagy, the exact interaction of polyphenols with autophagy markers is not known. These data require further research and will be beneficial in supporting polyphenol supplementation as a potential alternative treatment for regulating autophagy in neurodegenerative diseases.

摘要

多酚是植物来源的次生代谢物,具有广泛的治疗益处。它们也被报道为自噬、炎症和神经退行性变的调节剂。自噬途径对于降解过时的细胞器、蛋白质和其他细胞废物至关重要。自噬的失调会导致蛋白病、线粒体功能障碍和神经炎症,从而导致神经退行性变。有证据表明,多酚通过清除神经元中的错误折叠蛋白、抑制神经炎症和氧化应激以及防止神经退行性变来改善自噬。本综述试图总结多酚调节自噬的作用机制及其在 mTOR、AMPK、SIRT-1 和 ERK 等途径中的作用。多酚会增加自噬蛋白的水平,如 beclin-1、微管相关蛋白轻链 (LC3 I 和 II)、sirtuin 1 (SIRT1) 等,这一点是显而易见的。尽管多酚可以调节自噬,但多酚与自噬标志物的确切相互作用尚不清楚。这些数据需要进一步研究,将有助于支持多酚补充作为调节神经退行性疾病中自噬的潜在替代治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/e98d01a404ab/biomolecules-13-01196-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/e242edb210a3/biomolecules-13-01196-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/48c6b8c7d2e6/biomolecules-13-01196-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/3f2f8c2e8a32/biomolecules-13-01196-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/e98d01a404ab/biomolecules-13-01196-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/e242edb210a3/biomolecules-13-01196-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/48c6b8c7d2e6/biomolecules-13-01196-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/3f2f8c2e8a32/biomolecules-13-01196-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/10452370/e98d01a404ab/biomolecules-13-01196-g004.jpg

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Chemosphere. 2022 Nov;307(Pt 3):136020. doi: 10.1016/j.chemosphere.2022.136020. Epub 2022 Aug 16.
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Antioxidants (Basel). 2025 Feb 28;14(3):302. doi: 10.3390/antiox14030302.
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