Monotropein Improves Dexamethasone-Induced Muscle Atrophy via the AKT/mTOR/FOXO3a Signaling Pathways.
Piao Wang, Seok Yong Kang, Su Jin Kim, Yong-Ki Park, Hyo Won Jung
Author Information
Piao Wang: Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju 38066, Korea. ORCID
Seok Yong Kang: Korean Medicine R&D Center, Dongguk University, Gyeongju 38066, Korea.
Su Jin Kim: Department of Anesthesiology and Pain Medicine, College of Medicine, Dongguk University, Gyeongju 38066, Korea.
Yong-Ki Park: Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju 38066, Korea.
Hyo Won Jung: Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju 38066, Korea.
中文译文
English
The present study aimed to investigate the effects of monotropein (MON) on improving dexamethasone (DEX)-induced muscle atrophy in mice and C2C12 mouse skeletal muscle cells. The body weights, grip strengths, and muscle weights of mice were assessed. The histological change in the gastrocnemius tissues was also observed through H&E staining. The expression of myosin heavy chain (MyHC), muscle ring finger 1 (MuRF1), and muscle atrophy F-box (Atrogin1) and the phosphorylation of AKT, mTOR, and FOXO3a in the muscle tissues of mice and C2C12 myotubes were analyzed using Western blotting. MON improved muscle atrophy in mice and C2C12 myotubes by regulating catabolic states via the AKT/mTOR/FOXO3a signaling pathways, and enhanced muscle function by the increases of muscle mass and strength in mice. This suggests that MON could be used for the prevention and treatment of muscle atrophy in patients.
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2021R1A2C1012267/National Research Foundation of Korea
Dexamethasone
Humans
Iridoids
Muscle Fibers, Skeletal
Muscle, Skeletal
Muscular Atrophy
Proto-Oncogene Proteins c-akt
Signal Transduction
TOR Serine-Threonine Kinases
Ubiquitin-Protein Ligases
Iridoids
monotropein
Dexamethasone
Ubiquitin-Protein Ligases
MTOR protein, human
Proto-Oncogene Proteins c-akt
TOR Serine-Threonine Kinases