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通过 PI3K 介导的 Akt/mTOR 信号通路磷酸化增强肌管肥大。

Enhances Myotube Hypertrophy through PI3K-Mediated Akt/mTOR Signaling Phosphorylation.

机构信息

School of Public Health, Nantong University, Nantong 226019, China.

College of Physical Education, Hubei Normal University, Huangshi 435002, China.

出版信息

Nutrients. 2022 Apr 17;14(8):1670. doi: 10.3390/nu14081670.

DOI:10.3390/nu14081670
PMID:35458232
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9028211/
Abstract

Astragalus membranaceus (AM) is classified as a high-class traditional herbal medicine, which has strengthened vitality and multifunctional pharmacological activities, but limited empirical evidence is available to support its effects in muscular hypertrophy. It evokes skeletal muscle hypertrophy by increasing anabolic pathway, which is essential to prevent sarcopenia in elderly population. In this study, we examined the effects of AM on skeletal muscle hypertrophy by focusing on the molecular mechanism. We employed an in vitro model to investigate whether AM-treated skeletal muscle, as represented by myotube C2C12 cells, was hypertrophic, and to further investigate the efficacy of AM-activated phosphorylation of PI3K/Akt/mTOR signaling that must occur prior to myotube hypertrophy. The results showed that the myotubes formed larger multinucleated myotubes with increased diameter and thickness (1.16-fold relative to control group, p < 0.05). Administration of PI3K and mTOR inhibitors abolished AM-induced muscular hypertrophy. Moreover, AM-induced PI3K-mediated myotube hypertrophy was accompanied by the activation of Akt and mTOR signaling. We concluded that the AM is a nutritional activator to enhance muscular hypertrophy by increasing PI3K/Akt/mTOR signaling phosphorylation. As the AM is effective in myotube hypertrophy, AM and its derivatives may be promising candidates for ergogenic aid to prevent sarcopenia.

摘要

黄芪(AM)被归类为高级传统草药,具有增强生命力和多功能药理活性,但支持其在肌肉肥大方面的功效的经验证据有限。它通过增加合成代谢途径来引起骨骼肌肥大,这对于预防老年人群的肌肉减少症至关重要。在这项研究中,我们通过关注分子机制来研究 AM 对骨骼肌肥大的影响。我们采用体外模型来研究 AM 处理的骨骼肌(以肌管 C2C12 细胞为代表)是否肥大,并进一步研究 AM 激活的 PI3K/Akt/mTOR 信号转导的功效,该信号转导必须在肌管肥大之前发生。结果表明,肌管形成了更大的多核肌管,直径和厚度增加(相对对照组增加了 1.16 倍,p < 0.05)。施用 PI3K 和 mTOR 抑制剂可消除 AM 诱导的肌肉肥大。此外,AM 诱导的 PI3K 介导的肌管肥大伴随着 Akt 和 mTOR 信号的激活。我们得出结论,AM 是一种营养激活剂,通过增加 PI3K/Akt/mTOR 信号转导磷酸化来增强肌肉肥大。由于 AM 对肌管肥大有效,因此 AM 及其衍生物可能是预防肌肉减少症的有前途的运动补剂候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/9028211/ca059a49d8b5/nutrients-14-01670-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/9028211/915453cccfc7/nutrients-14-01670-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/9028211/44a72857a441/nutrients-14-01670-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/9028211/ca059a49d8b5/nutrients-14-01670-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/9028211/915453cccfc7/nutrients-14-01670-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/9028211/44a72857a441/nutrients-14-01670-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/9028211/ca059a49d8b5/nutrients-14-01670-g003.jpg

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