Area of Science:

• Biochemistry
• Cell Biology
• Pharmacology

Background:

• Dexamethasone (DEX) induces muscle atrophy, leading to decreased muscle mass and function.
• Understanding the molecular mechanisms of DEX-induced muscle atrophy is crucial for developing effective interventions.
• Pyropia yezoensis crude protein (PYCP) is a potential candidate for mitigating muscle wasting.

Purpose of the Study:

• To investigate the protective effects of PYCP against DEX-induced myotube atrophy in mice.
• To elucidate the underlying molecular mechanisms of PYCP's action.
• To evaluate PYCP as a potential therapeutic agent for muscle atrophy.

Main Methods:

• Mice were administered DEX and varying doses of PYCP orally for 18 days.
• Evaluated body weight, muscle weight (gastrocnemius, tibialis anterior), and calf thickness.
• Assessed serum markers (glucose, creatine kinase, lactate dehydrogenase) and key signaling pathways (IGF-I/Akt/mTOR/FOXO).
• Investigated the impact of PYCP on ubiquitin-proteasome and autophagy-lysosome pathways.

Main Results:

• PYCP significantly prevented DEX-induced reductions in body weight, calf thickness, and muscle mass.
• PYCP attenuated elevated serum glucose, creatine kinase, and lactate dehydrogenase levels.
• PYCP reversed muscle atrophy by regulating the IGF-I/Akt/mTOR/FOXO signaling pathway.
• PYCP inhibited both the ubiquitin-proteasome and autophagy-lysosome degradation pathways.

Conclusions:

• PYCP demonstrates significant protective effects against DEX-induced muscle atrophy.
• PYCP acts by promoting protein synthesis and inhibiting protein breakdown.
• PYCP supplementation is a promising strategy for preventing and treating muscle atrophy.