人参皂苷Rg5通过p38MAPK和Akt/mTOR信号通路促进肌肉再生

IF 6.8 2区 医学 Q1 CHEMISTRY, MEDICINAL
Ryuni Kim , Jee Won Kim , Hyerim Choi , Ji-Eun Oh , Tae Hyun Kim , Ga-Yeon Go , Sang-Jin Lee , Gyu-Un Bae
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引用次数: 0

摘要

骨骼肌在身体活动和能量代谢中起着关键作用。骨骼肌质量的减少会导致新陈代谢和身体活动方面的问题。目前正在进行研究,通过增加肌肉的质量和再生能力来预防这些疾病。据报道,人参皂苷Rg5具有广泛的药理活性。然而,关于Rg5对肌肉分化和生长影响的研究很少。方法采用诱导C2C12成肌细胞向Rg5分化,免疫印迹、免疫染色和qRT-PCR检测成肌标志物和前肌生成信号(p38MAPK),研究Rg5对成肌的影响。免疫沉淀证实Rg5通过p38MAPK增加了MyoD和E2A之间的相互作用。采用地塞米松诱导C2C12肌管肌萎缩的方法,探讨Rg5对肌质量损失的预防作用。对肌源性标志物、Akt/mTOR蛋白合成信号通路和萎缩相关基因(atrogin1和MuRF1)进行免疫印迹、免疫染色和qRT-PCR检测。结果rg5通过磷酸化p38MAPK和MyoD/E2A异源二聚化促进C2C12成肌细胞分化。此外,Rg5通过磷酸化Akt/mTOR刺激C2C12肌管肥大。Akt磷酸化诱导FoxO3a磷酸化,从而降低Atrogin-1和MuRF1的表达。结论Rg5促进肌肉发生和肥厚,预防地塞米松诱导的肌肉萎缩。据我们所知,这项研究首次表明Rg5促进肌肉再生,并表明Rg5可用于肌肉无力和萎缩的治疗干预,包括癌症恶病质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ginsenoside Rg5 promotes muscle regeneration via p38MAPK and Akt/mTOR signaling

Ginsenoside Rg5 promotes muscle regeneration via p38MAPK and Akt/mTOR signaling

Background

Skeletal muscles play a key role in physical activity and energy metabolism. The loss of skeletal muscle mass can cause problems related to metabolism and physical activity. Studies are being conducted to prevent such diseases by increasing the mass and regeneration capacity of muscles. Ginsenoside Rg5 has been reported to exhibit a broad range of pharmacological activities. However, studies on the effects of Rg5 on muscle differentiation and growth are scarce.

Methods

To investigate the effects of Rg5 on myogenesis, C2C12 myoblasts were induced to differentiate with Rg5, followed by immunoblotting, immunostaining, and qRT-PCR for myogenic markers and promyogenic signaling (p38MAPK). Immunoprecipitation confirmed that Rg5 increased the interaction between MyoD and E2A via p38MAPK. To investigate the effects of Rg5 on prevention of muscle mass loss, C2C12 myotubes were treated with dexamethasone to induce muscle atrophy. Immunoblotting, immunostaining, and qRT-PCR were performed for myogenic markers, Akt/mTOR signaling for protein synthesis, and atrophy-related genes (Atrogin-1 and MuRF1).

Results

Rg5 promoted C2C12 myoblast differentiation through phosphorylation of p38MAPK and MyoD/E2A heterodimerization. Furthermore, Rg5 stimulated C2C12 myotube hypertrophy via phosphorylation of Akt/mTOR. Phosphorylation of Akt induces FoxO3a phosphorylation, which reduces the expression of Atrogin-1 and MuRF1.

Conclusion

This study provides an understanding of how Rg5 promotes myogenesis and hypertrophy and prevents dexamethasone-induced muscle atrophy. The study is the first, to the best of our knowledge, to show that Rg5 promotes muscle regeneration and to suggest that Rg5 can be used for therapeutic intervention of muscle weakness and atrophy, including cancer cachexia.

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来源期刊
Journal of Ginseng Research
Journal of Ginseng Research CHEMISTRY, MEDICINAL-INTEGRATIVE & COMPLEMENTARY MEDICINE
CiteScore
11.40
自引率
9.50%
发文量
111
审稿时长
6-12 weeks
期刊介绍: Journal of Ginseng Research (JGR) is an official, open access journal of the Korean Society of Ginseng and is the only international journal publishing scholarly reports on ginseng research in the world. The journal is a bimonthly peer-reviewed publication featuring high-quality studies related to basic, pre-clinical, and clinical researches on ginseng to reflect recent progresses in ginseng research. JGR publishes papers, either experimental or theoretical, that advance our understanding of ginseng science, including plant sciences, biology, chemistry, pharmacology, toxicology, pharmacokinetics, veterinary medicine, biochemistry, manufacture, and clinical study of ginseng since 1976. It also includes the new paradigm of integrative research, covering alternative medicinal approaches. Article types considered for publication include review articles, original research articles, and brief reports. JGR helps researchers to understand mechanisms for traditional efficacy of ginseng and to put their clinical evidence together. It provides balanced information on basic science and clinical applications to researchers, manufacturers, practitioners, teachers, scholars, and medical doctors.
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