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首页> 外文期刊>Cell biology international. >Sulforaphane ameliorates serum starvation-induced muscle atrophy via activation of the Nrf2 pathway in cultured C2C12 cells
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Sulforaphane ameliorates serum starvation-induced muscle atrophy via activation of the Nrf2 pathway in cultured C2C12 cells

机译：亚磺烷烃通过培养的C2C12细胞的NRF2途径激活NRF2途径改善血清饥饿诱导的肌肉萎缩

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Oxidative stress, an imbalance of redox homeostasis, contributes to the pathogenesis and progress of muscle atrophy. However, it is debated whether oxidative stress is a cause or consequence of muscle atrophy. In this study, we investigated the relationship between menadione-induced oxidative stress and serum starvation-induced muscle atrophy in C2C12 myotubes. We found that atrophic phenotypes including myotube diameter decrease, protein ubiquitination, and the expression of atrogenes were detected under oxidative stress as well as during serum starvation. Oxidative stress during serum starvation was assessed to confirm the correlation. Both intracellular reactive oxygen species (ROS) and protein oxidation were increased in atrophic myotubes. These results indicate that menadione-induced oxidative stress triggers muscle atrophy and vice versa. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator of cellular response to oxidative stress and it is considered to have a cytoprotective role in the mitigation of muscle atrophy. Transcription of heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase-1, target genes of Nrf2, was decreased during serum starvation, which is related to decreased nuclear translocation of Nrf2. Pre-treatment of sulforaphane (SFN), a known Nrf2 inducer, before serum starvation showed a protective effect via Nrf2/HO-1 upregulation. SFN can liberate Nrf2 from Keap1, enabling the nuclear translocation of Nrf2. Consequently, the expression of HO-1 increased and intracellular ROS was significantly reduced by SFN pre-treatment. These results demonstrate that oxidative stress mediates the pathophysiology of muscle atrophy, which can be improved via upregulation of the Nrf2-mediated antioxidant response.
机译：氧化应激是一种氧化还原稳态失衡，参与了肌肉萎缩的发病机制和进展。然而，氧化应激是肌肉萎缩的原因还是后果仍存在争议。在本研究中，我们研究了甲萘醌诱导的氧化应激与血清饥饿诱导的C2C12肌管肌肉萎缩之间的关系。我们发现，在氧化应激和血清饥饿条件下均可检测到萎缩表型，包括肌管直径减小、蛋白质泛素化和萎缩基因的表达。评估血清饥饿期间的氧化应激，以确认这种相关性。萎缩的肌管细胞内活性氧（ROS）和蛋白质氧化均增加。这些结果表明，甲萘醌诱导的氧化应激会引发肌肉萎缩，反之亦然。核因子红系2相关因子2（Nrf2）是细胞对氧化应激反应的关键调节因子，被认为在缓解肌肉萎缩方面具有细胞保护作用。在血清饥饿期间，Nrf2靶基因血红素加氧酶-1（HO-1）和NAD（P）H醌脱氢酶-1的转录降低，这与Nrf2的核易位减少有关。在血清饥饿之前，已知的Nrf2诱导剂萝卜硫素（SFN）的预处理通过Nrf2/HO-1上调显示出保护作用。SFN可以将Nrf2从Keap1中释放出来，使Nrf2能够进行核移位。因此，SFN预处理后HO-1表达增加，细胞内ROS显著减少。这些结果表明，氧化应激介导了肌肉萎缩的病理生理学，这可以通过上调Nrf2介导的抗氧化反应来改善。

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