Abstract：
This study investigated the protective effect of carnosine and its components (L-histidine and β-alanine [HA]) against dexamethasone (Dex)-induced muscle atrophy in C2C12 myotubes. Myotubes were treated with Dex (10 μM) to induce muscle atrophy manifested by decreased myotube diameter, low myosin heavy chain content, and increased expression of muscle atrophy-associated ubiquitin ligases (Atrogin-1, MuRF-1, and Cbl-b). Carnosine (20 mM) treatment significantly improved the myotube diameter and MyHC protein expression level in Dex-treated C2C12 myotubes. It also downregulated the expression of Atrogin-1, MuRF-1, and Cbl-b and suppressed the expression of forkhead box O3 (FoxO3a) mediated by Dex. Furthermore, reactive oxygen species production was increased by Dex but was ameliorated by carnosine treatment. However, HA (20 mM), the component of carnosine, treatment was found ineffective in preventing Dex-induced protein damage. Therefore, based on above results it can be suggested that carnosine could be a potential therapeutic agent to prevent Dex-induced muscle atrophy compared to its components HA.
摘要：
这项研究调查了肌肽及其成分（L-组氨酸和β-丙氨酸[HA]）对地塞米松（Dex）诱导的C2C12肌管肌肉萎缩的保护作用。用Dex（10μM）处理肌管以诱导表现为肌管直径减小的肌肉萎缩，低肌球蛋白重链含量，和肌肉萎缩相关的泛素连接酶（Atrogin-1，MuRF-1和Cbl-b）的表达增加。肌肽(20mM)处理显著改善Dex处理的C2C12肌管中的肌管直径和MyHC蛋白表达水平。它还下调了Atrogin-1，MuRF-1和Cbl-b的表达，并抑制了Dex介导的叉头盒O3（FoxO3a）的表达。此外，Dex增加了活性氧的产生，但肌肽处理改善了活性氧的产生。然而,HA(20mM),肌肽的成分，发现治疗在预防Dex诱导的蛋白质损伤方面无效。因此,基于上述结果,可以表明肌肽与其组分HA相比可能是预防Dex诱导的肌肉萎缩的潜在治疗剂。
