Polyphenols and their potential role in preventing skeletal muscle atrophy

被引:55
|
作者
Salucci, Sara [1 ]
Falcieri, Elisabetta [1 ]
机构
[1] Univ Urbino Carlo Bo, Dept Biomol Sci, Urbino, Italy
关键词
P-COUMARIC ACID; OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; PHYSICAL-EXERCISE; RESVERATROL PREVENTS; SIGNALING PATHWAYS; PROTEIN-SYNTHESIS; GENE-EXPRESSION; DNA-DAMAGE; OLIVE OIL;
D O I
10.1016/j.nutres.2019.11.004
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Skeletal muscle atrophy is the consequence of various conditions, such as disuse, denervation, fasting, aging, and disease. Even if the underlying molecular mechanisms are still not fully understood, an elevated oxidative stress related to mitochondrial dysfunction has been proposed as one of the major contributors to skeletal muscle atrophy. Researchers have described various forms of nutritional supplementation to prevent oxidative stress-induced muscle wasting. Among a variety of nutrients, attention has also focused on polyphenols, a wide range of plant-based compounds with antioxidant and inflammatory properties, many of which have beneficial effects on human health and might retard skeletal muscle loss and function impairment. The purpose of this review is to describe polyphenol actions in skeletal muscle atrophy prevention. Published articles from the last 10 years were searched on PubMed and other databases. Polyphenols are important molecules that should be considered when discussing possible strategies against muscle atrophy. In particular, the collected studies describe, for each polyphenol subclass, the beneficial effect on muscle mass preservation in various skeletal muscle disorders. In these examples, the polyphenol compounds appear to mainly act by reversing mitochondrial dysfunction. Given that the current information on polyphenols is mostly restricted to basic studies, more comprehensive research and additional studies should be performed to clarify their mechanisms of action in improving skeletal muscle functions during atrophy. (C) 2019 Elsevier Inc. All rights reserved.
引用
收藏
页码:10 / 22
页数:13
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