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岩藻黄质可挽救地塞米松诱导的 C2C12 肌管萎缩。

Fucoxanthin rescues dexamethasone induced C2C12 myotubes atrophy.

机构信息

Department of Geriatrics, the First Affiliated Hospital of Chongqing Medical University, China.

出版信息

Biomed Pharmacother. 2021 Jul;139:111590. doi: 10.1016/j.biopha.2021.111590. Epub 2021 Apr 14.

Abstract

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.

摘要

肌肉萎缩和无力是长期或大剂量使用糖皮质激素的不良反应。在本研究中,我们探讨了岩藻黄质(10μM)对 C2C12 肌管中地塞米松(10μM)诱导的萎缩的影响,并研究了其潜在机制。在光镜下观察肌管的直径,并通过 Western blot 或免疫沉淀分析肌球蛋白重链(MyHC)、蛋白水解相关、自噬相关、凋亡相关和线粒体相关蛋白的表达。岩藻黄质可减轻 C2C12 肌管中的地塞米松诱导的肌肉萎缩,表现为肌管直径增加和 MyHC 表达增加,肌肉萎缩 F -box(Atrogin-1)和肌肉环指 1(MuRF1)表达降低。通过激活 SIRT1,岩藻黄质抑制叉头框 O(FoxO)转录活性以减少蛋白质降解,诱导自噬以增强降解蛋白的清除,促进线粒体功能并减少凋亡。总之,我们发现岩藻黄质通过激活 SIRT1 改善地塞米松诱导的 C2C12 肌管萎缩。

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