Muscle atrophy, a debilitating condition characterized by loss of muscle mass and strength, is a major concern in various clinical settings. Acetyl genistin (AG), a bioactive compound, was evaluated for its role in muscle cell differentiation and its potential protective effects against dexamethasone (dexa)-induced muscle atrophy. Our study demonstrated that AG significantly promoted C2C12 myotube differentiation, as evidenced by enhanced myotube width and increased fusion index. Notably, AG treatment upregulated the expression of myogenic markers, including MHC, MyoD, and MyoG. Moreover, AG displayed protective properties by attenuating dexa-induced muscle atrophy, mainly by suppressing the expression of the atrophy-related genes MAFbx and MuRF1. AG's protective effects are mechanistically attributed to its regulation of the AMPK/FoxO-dependent signaling pathway. Our results highlighted the dual benefits of AG in fostering muscle differentiation and safeguarding against muscle atrophy, positioning it as a promising agent for muscle health and therapeutic applications.

中文翻译：

---

乙酰基染料木苷通过 C2C12 肌管中的 FoxO1/3 信号通路调节肌管分化并减轻地塞米松诱导的肌肉萎缩

肌肉萎缩是一种以肌肉质量和力量丧失为特征的衰弱病症，是各种临床环境中的主要问题。乙酰染料木苷 (AG) 是一种生物活性化合物，对其在肌肉细胞分化中的作用及其对地塞米松 (dexa) 诱导的肌肉萎缩的潜在保护作用进行了评估。我们的研究表明，AG 显着促进 C2C12 肌管分化，肌管宽度增加和融合指数增加证明了这一点。值得注意的是，AG 治疗上调了肌源性标志物的表达，包括 MHC、MyoD 和 MyoG。此外，AG 通过减轻 dexa 诱导的肌肉萎缩（主要是通过抑制萎缩相关基因 MAFbx 和 MuRF1 的表达）来表现出保护特性。AG 的保护作用在机制上归因于其对 AMPK/FoxO 依赖性信号通路的调节。我们的结果强调了 AG 在促进肌肉分化和防止肌肉萎缩方面的双重益处，使其成为肌肉健康和治疗应用的有前途的药物。