Scholarlink

<p>This study investigated whether a fucosterol-standardized <i>Sargassum fulvellum</i> extract (SFE) attenuates muscle atrophy by regulating inflammatory responses and muscle protein turnover in vitro and in vivo. In tumor necrosis factor-α–stimulated C2C12 myotubes, SFE suppressed inflammatory cytokine expression (<i>Tnf</i> and <i>Il6</i>) and attenuated protein degradation by downregulating muscle-specific ubiquitin ligases (<i>Trim63</i> and <i>Fbxo32</i>) via restored forkhead box O3a phosphorylation. SFE also restored myogenic regulatory factors (<i>Myod1</i> and <i>Myog</i>) and reactivated the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) signaling pathway, indicating recovery of anabolic signaling. In immobilization-induced muscle atrophy mice, SFE improved grip strength and preserved skeletal muscle mass, accompanied by an increase in muscle fiber cross-sectional area. At the molecular level, SFE mitigated inflammatory responses and restored imbalance between protein synthesis and degradation in the tibialis anterior muscle. Collectively, these findings demonstrate that SFE attenuates immobilization-induced muscle atrophy by suppressing inflammation and restoring PI3K/Akt/mTOR-mediated muscle protein homeostasis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Fucosterol-standardized extract of Sargassum fulvellum attenuates immobilization-induced skeletal muscle atrophy via PI3K/Akt/mTOR signaling

  • 期刊论文

  • 发表日期：

    2026年5月29日

查看全文
  • Mi-Bo Kim,
  • Jieun Hwang,
  • Hyunju Kang,
  • Chae Young Moon,
  • Lei Cao,
  • Jae-Kwan Hwang

摘要

This study investigated whether a fucosterol-standardized Sargassum fulvellum extract (SFE) attenuates muscle atrophy by regulating inflammatory responses and muscle protein turnover in vitro and in vivo. In tumor necrosis factor-α–stimulated C2C12 myotubes, SFE suppressed inflammatory cytokine expression (Tnf and Il6) and attenuated protein degradation by downregulating muscle-specific ubiquitin ligases (Trim63 and Fbxo32) via restored forkhead box O3a phosphorylation. SFE also restored myogenic regulatory factors (Myod1 and Myog) and reactivated the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) signaling pathway, indicating recovery of anabolic signaling. In immobilization-induced muscle atrophy mice, SFE improved grip strength and preserved skeletal muscle mass, accompanied by an increase in muscle fiber cross-sectional area. At the molecular level, SFE mitigated inflammatory responses and restored imbalance between protein synthesis and degradation in the tibialis anterior muscle. Collectively, these findings demonstrate that SFE attenuates immobilization-induced muscle atrophy by suppressing inflammation and restoring PI3K/Akt/mTOR-mediated muscle protein homeostasis.