肌发生
肌肉萎缩
C2C12型
岩藻黄质
萎缩
自噬
MG132型
内科学
内分泌学
生物
心肌细胞
细胞凋亡
化学
细胞生物学
蛋白酶体抑制剂
生物化学
医学
类胡萝卜素
作者
Zhiyin Liao,Jinliang Chen,Qiunan Chen,Yang Yunfei,Qian Xiao
标识
DOI:10.1016/j.biopha.2021.111590
摘要
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.
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