Yeo Changhwan, Kim Hyunseong, Jeon Wan-Jin, Lee Junseon, Hong Jin Young, Kim Hyun, Lee Yoon Jae, Baek Seung Ho, Ha In-Hyuk
Jaseng Spine and Joint Research Institute, Jaseng Medical Foundation, Seoul, 135-896, Republic of Korea.
College of Korean Medicine, Dongguk University, 32, Dongguk-ro, Ilsandong-gu, Goyang-si, 10326, Gyeonggi-do, Republic of Korea.
J Muscle Res Cell Motil. 2024 Mar;45(1):1-10. doi: 10.1007/s10974-023-09661-5. Epub 2023 Oct 17.
Glucocorticoids (GCs) are commonly used in the treatment of chronic inflammatory conditions. However, the administration of high doses and long-term use of GCs can induce muscle atrophy (MA) in patients, leading to a decline in quality of life and increased mortality. MA leads to protein degradation in skeletal muscle, resulting in a reduction of muscle mass. This process is triggered by GCs like dexamethasone (DEX), which induce the expression of E3 ubiquitin ligases, namely Atrogin-1 and muscle RING-finger protein-1 (MuRF1). In this study, we examined the anti-MA potential of Luffa cylindrica Roemer (LCR) on DEX-treated primary skeletal myotubes. Primary skeletal myotubes stimulated with LCR alone resulted in a significant upregulation of myotube development, characterized by an increase in both the number and diameter of myotubes. Contrastingly, combined treatment with LCR and DEX reduced the expression of Atrogin-1, while treatment with DEX alone induced the expression of MuRF1. Furthermore, LCR treatment successfully restored the number and diameter of myotubes that had been diminished by DEX treatment. These findings suggest that LCR holds potential for treating MA, as an accelerating effect on muscle development and anti-MA effects on primary skeletal muscle cells were observed.
糖皮质激素(GCs)常用于治疗慢性炎症性疾病。然而,高剂量使用和长期使用GCs会导致患者出现肌肉萎缩(MA),进而导致生活质量下降和死亡率增加。MA会导致骨骼肌中的蛋白质降解,从而使肌肉质量减少。这个过程是由地塞米松(DEX)等GCs引发的,它们会诱导E3泛素连接酶即肌肉萎缩蛋白-1(Atrogin-1)和肌肉环状指蛋白-1(MuRF1)的表达。在本研究中,我们检测了丝瓜(LCR)对DEX处理的原代骨骼肌肌管的抗MA潜力。单独用LCR刺激原代骨骼肌肌管会导致肌管发育显著上调,其特征是肌管数量和直径均增加。相比之下,LCR与DEX联合处理可降低Atrogin-1的表达,而单独用DEX处理则会诱导MuRF1的表达。此外,LCR处理成功恢复了因DEX处理而减少的肌管数量和直径。这些发现表明,LCR具有治疗MA的潜力,因为观察到其对肌肉发育有促进作用且对原代骨骼肌细胞有抗MA作用。