Abstract
We investigated the protective effects of Pyropia yezoensis crude protein (PYCP) against dexamethasone (DEX)-induced myotube atrophy and its underlying mechanisms. DEX (3 mg/kg body weight, intraperitoneal injection) and PYCP (150 and 300 mg/kg body weight, oral) were administrated to mice for 18 days, and the effects of PYCP on DEX-induced muscle atrophy were evaluated. Body weight, calf thickness, and gastrocnemius and tibialis anterior muscle weight were significantly decreased by DEX administration (p < 0.05), while PYCP supplementation effectively prevented the DEX-induced decrease in body weight, calf thickness, and muscle weight. PYCP supplementation also attenuated the DEX-induced increase in serum glucose, creatine kinase, and lactate dehydrogenase levels. Additionally, PYCP supplementation reversed DEX-induced muscle atrophy via the regulation of the insulin-like growth factor-I/protein kinase B/rapamycin-sensitive mTOR complex I/forkhead box O signaling pathway. The mechanistic investigation revealed that PYCP inhibited the ubiquitin-proteasome and autophagy-lysosome pathways in DEX-administrated C57BL/6 mice. These findings demonstrated that PYCP increased protein synthesis and decreased protein breakdown to prevent muscle atrophy. Therefore, PYCP supplementation appears to be useful for preventing muscle atrophy.
Highlights
Skeletal muscle atrophy occurs in a variety of conditions, such as muscle inactivity, fasting, multiple disease states, age-related atrophy, and glucocorticoid (GC) treatment [1,2]
These findings demonstrated that Pyropia yezoensis crude protein (PYCP) increased protein synthesis and decreased protein breakdown to prevent muscle atrophy
PYCP supplementation effectively prevented the DEX-induced decrease in body weight (Table 1)
Summary
Skeletal muscle atrophy occurs in a variety of conditions, such as muscle inactivity (e.g., joint immobilization and prolonged bed rest), fasting, multiple disease states, age-related atrophy, and glucocorticoid (GC) treatment [1,2]. IGF-I increases protein synthesis by activating downstream targets of the PI3K/Akt/mTORC1 signaling pathway [14]. Recent studies have shown that the inhibition of mTORC1 complex by GC is induced by the transcription of the mTORC1 repressors regulated in development and DNA damage response 1 (REDD1) and Kruppel-like factor 15 (KLF-15) [18]. These findings suggest that GC-induced skeletal muscle atrophy could be mediated by a decrease in IGF-I/Akt/mTORC1 activity in skeletal muscle. Candidate mechanisms underlying the inhibition of skeletal muscle atrophy by Pyropia yezoensis crude protein (PYCP) supplementation were considered
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