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首页> 外文期刊>American Journal of Physiology >Sphingosine 1-phosphate protects mouse extensor digitorum longus skeletal muscle during fatigue.
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Sphingosine 1-phosphate protects mouse extensor digitorum longus skeletal muscle during fatigue.

机译：1-磷酸鞘氨醇可在疲劳期间保护小鼠伸指长肌骨骼肌。

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Sphingomyelin derivatives exert various second messenger actions in numerous tissues. Sphingosine (SPH) and sphingosine 1-phosphate (S1P) are two major sphingomyelin derivatives present at high levels in blood. The aim of the present work was to investigate whether S1P and SPH exert relevant actions in mouse skeletal muscle contractility and fatigue. Exogenous S1P and SPH administration caused a significant reduction of tension decline during fatigue of extensor digitorum longus muscle. Final tension after the fatiguing protocol was 40% higher than in untreated muscle. Interestingly, N,N-dimethylsphingosine, an inhibitor of SPH kinase (SK), abolished the effect of supplemented SPH but not that of S1P, suggesting that SPH acts through its conversion to S1P. Moreover, SPH was not effective in Ca(2+)-free solutions, in agreement with the hypothesis that SPH action is dependent on its conversion to S1P by the Ca(2+)-requiring enzyme SK. In contrast to SPH, S1P produced its positive effects on fatigue in Ca(2+)-free conditions, indicating that S1P action does not require Ca(2+) entry and most likely is receptor mediated. The effects of S1P could be ascribed in part to its ability to prevent the reduction (-20 mV) of action potential amplitude caused by fatigue. In conclusion, these results indicate that extracellular S1P has protective effects during the development of muscle fatigue and that the extracellular conversion of SPH to S1P may represent a rheostat mechanism to protect skeletal muscle from possible cytotoxic actions of SPH.
机译：鞘磷脂衍生物在许多组织中发挥各种第二信使作用。鞘氨醇（SPH）和1-磷酸鞘氨醇（S1P）是血液中高含量存在的两种主要鞘磷脂衍生物。本工作的目的是研究S1P和SPH是否在小鼠骨骼肌收缩力和疲劳中发挥相关作用。外用S1P和SPH给药可显着减少指趾长肌疲劳期间的紧张度下降。疲劳方案后的最终张力比未经治疗的肌肉高40％。有趣的是，SPH激酶（SK）的抑制剂N，N-二甲基鞘氨醇取消了补充的SPH的作用，但没有取消S1P的作用，这表明SPH通过转化为S1P起作用。此外，SPH在不含Ca（2+）的解决方案中无效，这与SPH的作用取决于需要Ca（2+）的酶SK转化为S1P的假设相一致。与SPH相反，S1P在无Ca（2+）的条件下对疲劳产生了积极的影响，表明S1P的作用不需要Ca（2+）进入，很可能是受体介导的。 S1P的作用可能部分归因于其防止疲劳引起的动作电位振幅降低（-20 mV）的能力。总之，这些结果表明细胞外S1P在肌肉疲劳的发展过程中具有保护作用，并且SPH向S1P的细胞外转化可能代表了变阻器机制，以保护骨骼肌免受SPH可能的细胞毒性作用。

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