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BST204,一种 Rg3 和 Rh2 富集的人参提取物,可上调 TNF-α 诱导的萎缩肌管中的肌管形成和线粒体功能。

BST204, a Rg3 and Rh2 Enriched Ginseng Extract, Upregulates Myotube Formation and Mitochondrial Function in TNF-α-Induced Atrophic Myotubes.

机构信息

Research Institute of Pharmaceutical Science, College of Pharmacy, Sookmyung Women's University, Seoul 04310, Republic of Korea.

Green Cross Wellbeing Co., Ltd., Seongnam 13595, Republic of Korea.

出版信息

Am J Chin Med. 2020;48(3):631-650. doi: 10.1142/S0192415X20500329. Epub 2020 Apr 24.

DOI:10.1142/S0192415X20500329
PMID:32329640
Abstract

The loss of skeletal muscle mass and function is a serious consequence of chronic diseases and aging. BST204 is a purified ginseng (the root of ) extract that has been processed using ginsenoside--glucosidase and acid hydrolysis to enrich ginsenosides Rg3 and Rh2 from the crude ginseng. BST204 has a broad range of health benefits, but its effects and mechanism on muscle atrophy are currently unknown. In this study, we have examined the effects and underlying mechanisms of BST204 on myotube formation and myotube atrophy induced by tumor necrosis factor- (TNF-). BST204 promotes myogenic differentiation and multinucleated myotube formation through Akt activation. BST204 prevents myotube atrophy induced by TNF- through the activation of Akt/mTOR signaling and down-regulation of muscle-specific ubiquitin ligases, MuRF1, and Atrogin-1. Furthermore, BST204 treatment in atrophic myotubes suppresses mitochondrial reactive oxygen species (ROS) production and regulates mitochondrial transcription factors such as NRF1 and Tfam, through enhancing the activity and expression of peroxisome proliferator-activated receptor- coactivator1 (PGC1). Collectively, our findings indicate that BST204 improves myotube formation and PGC1-mediated mitochondrial function, suggesting that BST204 is a potential therapeutic or neutraceutical remedy to intervene muscle weakness and atrophy.

摘要

骨骼肌质量和功能的丧失是慢性疾病和衰老的严重后果。BST204 是一种经过纯化的人参(根)提取物,经过人参皂苷-葡萄糖苷酶和酸水解处理,从粗人参中富集人参皂苷 Rg3 和 Rh2。BST204 具有广泛的健康益处,但它对肌肉萎缩的作用和机制目前尚不清楚。在这项研究中,我们研究了 BST204 对肿瘤坏死因子-(TNF-)诱导的肌管形成和肌管萎缩的作用及其潜在机制。BST204 通过激活 Akt 促进成肌分化和多核肌管形成。BST204 通过激活 Akt/mTOR 信号通路和下调肌肉特异性泛素连接酶 MuRF1 和 Atrogin-1 来预防 TNF-诱导的肌管萎缩。此外,BST204 在萎缩肌管中的治疗通过增强过氧化物酶体增殖物激活受体-共激活因子 1(PGC1)的活性和表达来抑制线粒体活性氧(ROS)的产生并调节核转录因子如 NRF1 和 Tfam。总之,我们的研究结果表明,BST204 可改善肌管形成和 PGC1 介导的线粒体功能,表明 BST204 是一种潜在的治疗或营养补救措施,可干预肌肉无力和萎缩。

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