Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju 38066, Korea.
Korean Medicine R&D Center, Dongguk University, Gyeongju 38066, Korea.
Nutrients. 2022 Apr 29;14(9):1859. doi: 10.3390/nu14091859.
The present study aimed to investigate the effects of monotropein (MON) on improving dexamethasone (DEX)-induced muscle atrophy in mice and C2C12 mouse skeletal muscle cells. The body weights, grip strengths, and muscle weights of mice were assessed. The histological change in the gastrocnemius tissues was also observed through H&E staining. The expression of myosin heavy chain (MyHC), muscle ring finger 1 (MuRF1), and muscle atrophy F-box (Atrogin1) and the phosphorylation of AKT, mTOR, and FOXO3a in the muscle tissues of mice and C2C12 myotubes were analyzed using Western blotting. MON improved muscle atrophy in mice and C2C12 myotubes by regulating catabolic states via the AKT/mTOR/FOXO3a signaling pathways, and enhanced muscle function by the increases of muscle mass and strength in mice. This suggests that MON could be used for the prevention and treatment of muscle atrophy in patients.
本研究旨在探讨麦角甾苷（MON）改善地塞米松（DEX）诱导的小鼠肌肉萎缩和 C2C12 鼠骨骼肌细胞萎缩的作用。评估了小鼠的体重、握力和肌肉重量。通过 H&E 染色观察了腓肠肌组织的组织学变化。使用 Western blot 分析了小鼠肌肉组织和 C2C12 肌管中肌球蛋白重链（MyHC）、肌肉环指 1（MuRF1）和肌肉萎缩 F 盒（Atrogin1）的表达以及肌肉组织中 AKT、mTOR 和 FOXO3a 的磷酸化。MON 通过调节 AKT/mTOR/FOXO3a 信号通路来改善小鼠和 C2C12 肌管中的肌肉萎缩，并通过增加小鼠的肌肉质量和力量来增强肌肉功能。这表明 MON 可用于预防和治疗患者的肌肉萎缩。
