Key result
Quercetin administration significantly enhanced the contractility of artificial skeletal muscle at week 2 (p<0.01) and promoted myotube formation via upregulation of Myh3 and cell migration by Cxcl5.
Why the study?
Direct muscle atrophy therapeutics are urgently needed, and global shifts toward non-animal testing require alternatives to animal studies for evaluating pharmaceutical and food-derived functional ingredients.
p-value: p=<0.01
Atrophy is characterized by muscle weakness and reduced mobility and results from inactivity, aging, cancer cachexia, and excessive glucocorticoid use. Skeletal muscle is essential for locomotion and energy production and accounts for a significant portion of body weight. Loss of muscle function adversely affects athletic performance and metabolism, affecting quality of life. Since there is no definitive cure, preventive measures such as diet and exercise are taken. The development of direct muscle atrophy therapeutics is urgently needed. Historically, animal studies have been used to predict pharmaceutical and food-derived functional ingredients efficacy in humans and to assess pharmacokinetics. However, in recent years there has been a global shift towards non-animal methods (alternatives to animal testing) due to animal welfare concerns. This study introduces a versatile assay for the development of Pharmaceutical and food-derived functional ingredients for the treatment of muscle atrophy using an artificial skeletal muscle contractility-based drug quantification platform. The effectiveness of this platform was demonstrated with quercetin, revealing its direct role in enhancing muscle contractility and promoting myotube formation via upregulation of Myh3 and cell migration by Cxcl5. This method provides a bridge between cellular assays and human studies and will advance research into the treatment of myopathies.
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KISHISHITA et al. (2023) studied Muscle atrophy. Quercetin vs. DMSO (1%) was evaluated on Muscle contractility (fold change) (p=<0.01). Quercetin administration significantly enhanced the contractility of artificial skeletal muscle at week 2 (p<0.01) and promoted myotube formation via upregulation of Myh3 and cell migration by Cxcl5.
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