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Abstract：
Epicatechin is a polyphenol compound that promotes skeletal muscle differentiation and counteracts the pathways that participate in the degradation of proteins. Several studies present contradictory results of treatment protocols and therapeutic effects. Therefore, the objective of this systematic review was to investigate the current literature showing the molecular mechanism and clinical protocol of epicatechin in muscle atrophy in humans, animals, and myoblast cell-line. The search was conducted in Embase, PubMed/MEDLINE, Cochrane Library, and Web of Science. The qualitative analysis demonstrated that there is a commonness of epicatechin inhibitory action in myostatin expression and atrogenes MAFbx, FOXO, and MuRF1. Epicatechin showed positive effects on follistatin and on the stimulation of factors related to the myogenic actions (MyoD, Myf5, and myogenin). Furthermore, the literature also showed that epicatechin can interfere with mitochondrias\' biosynthesis in muscle fibers, stimulation of the signaling pathways of AKT/mTOR protein production, and amelioration of skeletal musculature performance, particularly when combined with physical exercise. Epicatechin can, for these reasons, exhibit clinical applicability due to the beneficial results under conditions that negatively affect the skeletal musculature. However, there is no protocol standardization or enough clinical evidence to draw more specific conclusions on its therapeutic implementation.
摘要：
表儿茶素是一种多酚化合物，可促进骨骼肌分化并抵消参与蛋白质降解的途径。一些研究提出了治疗方案和治疗效果的矛盾结果。因此,本系统综述的目的是调查目前的文献显示表儿茶素在人类肌肉萎缩的分子机制和临床方案，动物,和成肌细胞细胞系。搜索是在Embase进行的,PubMed/MEDLINE,科克伦图书馆,和WebofScience。定性分析表明，表儿茶素在肌肉生长抑制素表达和atrogenesMAFbx中的抑制作用具有共性，FOXO,MuRF1表儿茶素对卵泡抑素和与肌源性作用相关的因素的刺激显示出积极作用（MyoD，Myf5和肌生成素）。此外，文献还表明，表儿茶素可以干扰肌肉纤维中线粒体的生物合成，刺激AKT/mTOR蛋白产生的信号通路，和改善骨骼肌性能，特别是与体育锻炼相结合时。表儿茶素可以，由于这些原因,由于在对骨骼肌系统产生负面影响的条件下的有益结果，因此表现出临床适用性。然而,没有方案标准化或足够的临床证据来得出关于其治疗实施的更具体结论.
