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首页> 外文期刊>American Journal of Physiology >Tumor necrosis factor-alpha inhibits myogenesis through redox-dependent and -independent pathways.
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Tumor necrosis factor-alpha inhibits myogenesis through redox-dependent and -independent pathways.

机译：肿瘤坏死因子-α通过氧化还原依赖性和非依赖性途径抑制肌发生。

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摘要

Muscle wasting accompanies diseases that are associated with chronic elevated levels of circulating inflammatory cytokines and oxidative stress. We previously demonstrated that tumor necrosis factor-alpha (TNF-alpha) inhibits myogenic differentiation via the activation of nuclear factor-kappaB (NF-kappaB). The goal of the present study was to determine whether this process depends on the induction of oxidative stress. We demonstrate here that TNF-alpha causes a decrease in reduced glutathione (GSH) during myogenic differentiation of C(2)C(12) cells, which coincides with an elevated generation of reactive oxygen species. Supplementation of cellular GSH with N-acetyl-l-cysteine (NAC) did not reverse the inhibitory effects of TNF-alpha on troponin I promoter activation and only partially restored creatine kinase activity in TNF-alpha-treated cells. In contrast, the administration of NAC before treatment with TNF-alpha almost completely restored the formation of multinucleated myotubes. NAC decreased TNF-alpha-induced activation of NF-kappaB only marginally, indicating that the redox-sensitive component of the inhibition of myogenic differentiation by TNF-alpha occurred independently, or downstream of NF-kappaB. Our observations suggest that the inhibitory effects of TNF-alpha on myogenesis can be uncoupled in a redox-sensitive component affecting myotube formation and a redox independent component affecting myogenic protein expression.
机译：肌肉消瘦伴随着与慢性炎症循环细胞因子水平升高和氧化应激相关的疾病。我们先前证明，肿瘤坏死因子-α（TNF-α）通过激活核因子-κB（NF-kappaB）抑制肌原性分化。本研究的目的是确定该过程是否取决于氧化应激的诱导。我们在这里证明，TNF-α导致减少的谷胱甘肽（GSH）在C（2）C（12）细胞的成肌分化过程中减少，这与活性氧的产生增加相吻合。用N-乙酰基-1-半胱氨酸（NAC）补充细胞GSH不能逆转TNF-α对肌钙蛋白I启动子活化的抑制作用，而只能部分恢复TNF-α处理的细胞中的肌酸激酶活性。相反，在用TNF-α治疗之前给予NAC几乎完全恢复了多核肌管的形成。 NAC仅轻微地降低了TNF-α诱导的NF-κB的激活，这表明由TNF-α抑制肌原性分化的氧化还原敏感成分独立发生，或在NF-κB的下游发生。我们的观察结果表明，TNF-α对肌发生的抑制作用可以在影响肌管形成的氧化还原敏感成分和影响肌原蛋白表达的氧化还原独立成分中解偶联。

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