Fucoxanthin rescues dexamethasone induced C2C12 myotubes atrophy
Autor: | Yang Yunfei, Xiao Qian, Chen Jinliang, Liao Zhiyin, Chen Qiunan |
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Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Cell Survival Fucoxanthin Muscle Fibers Skeletal Apoptosis RM1-950 Xanthophylls Protein degradation Dexamethasone Cell Line Mice 03 medical and health sciences chemistry.chemical_compound SIRT1 0302 clinical medicine Atrophy Sirtuin 1 Myosin Autophagy medicine Animals Pharmacology Myogenesis Forkhead Box Protein O3 General Medicine medicine.disease Muscle atrophy Cell biology 030104 developmental biology chemistry 030220 oncology & carcinogenesis C2C12 Therapeutics. Pharmacology medicine.symptom Proto-Oncogene Proteins c-akt |
Zdroj: | Biomedicine & Pharmacotherapy, Vol 139, Iss, Pp 111590-(2021) |
ISSN: | 0753-3322 |
Popis: | Muscle atrophy and weakness are the adverse effects of long-term or high dose usage of glucocorticoids. In the present study, we explored the effects of fucoxanthin (10 μM) on dexamethasone (10 μM)-induced atrophy in C2C12 myotubes and investigated its underlying mechanisms. The diameter of myotubes was observed under a light microscope, and the expression of myosin heavy chain (MyHC), proteolysis-related, autophagy-related, apoptosis-related, and mitochondria-related proteins was analyzed by western blots or immunoprecipitation. Fucoxanthin alleviates dexamethasone-induced muscle atrophy in C2C12 myotubes, indicated by increased myotubes diameter and expression of MyHC, decreased expression of muscle atrophy F-box (Atrogin-1) and muscle ring finger 1 (MuRF1). Through activating SIRT1, fucoxanthin inhibits forkhead box O (FoxO) transcriptional activity to reduce protein degradation, induces autophagy to enhance degraded protein clearance, promotes mitochondrial function and diminishes apoptosis. In conclusion, we identified fucoxanthin ameliorates dexamethasone induced C2C12 myotubes atrophy through SIRT1 activation. |
Databáze: | OpenAIRE |
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