Mealworm Ethanol Extract Enhances Myogenic Differentiation and Alleviates Dexamethasone-Induced Muscle Atrophy in C2C12 Cells.
Ra-Yeong ChoiBong Sun KimEu-Jin BanMinchul SeoJoon Ha LeeIn-Woo KimPublished in: Life (Basel, Switzerland) (2022)
Aging, and other disease-related muscle disorders are serious health problems. Dexamethasone (DEX), a synthetic glucocorticoid, can trigger skeletal muscle atrophy. This study examined the effects of mealworm ( Tenebrio molitor larva) ethanol extract (TME) on C2C12 myoblast differentiation and DEX-induced myotube atrophy. TME induced myotube formation compared to the differentiation medium (DM) group. TME also significantly increased the mRNA expression of muscle creatine kinase ( CKm ) and myogenic regulatory factors (MRFs), such as myogenin ( MyoG ), myogenic factor ( Myf )5, and MRF4 ( Myf6 ). TME dramatically increased the muscle-specific protein, MyoG, compared to the control, whereas the expression of myogenic differentiation 1 (MyoD) remained unchanged. It also activated the mammalian target of rapamycin (mTOR) signaling pathway. In the DEX-induced muscle atrophy C2C12 model, TME reduced the gene expression of atrogin-1 , muscle RING finger protein-1 ( MuRF-1 ), and myostatin , which are involved in protein degradation in skeletal muscles. Furthermore, TME elevated the phosphorylation of forkhead box O3 (FoxO3α) and protein kinase B (Akt). These findings suggest that TME can enhance myotube hypertrophy by regulating the mTOR signaling pathway, and can rescue DEX-induced muscle atrophy by alleviating atrophic muscle markers mediated by Akt activation. Thus, TME can be a potential therapeutic agent for treating muscle weakness and atrophy.
Keyphrases
- skeletal muscle
- signaling pathway
- high glucose
- diabetic rats
- gene expression
- insulin resistance
- cell proliferation
- transcription factor
- induced apoptosis
- protein kinase
- healthcare
- drug induced
- mental health
- pi k akt
- public health
- oxidative stress
- type diabetes
- low dose
- endothelial cells
- dna methylation
- small molecule
- poor prognosis
- tyrosine kinase
- endoplasmic reticulum stress
- amino acid
- social media
- climate change
- cell cycle arrest
- anti inflammatory