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首页> 外文期刊>Journal of Muscle Research and Cell Motility >Stretching and electrical stimulation reduce the accumulation of MyoD, myostatin and atrogin-1 in denervated rat skeletal muscle
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Stretching and electrical stimulation reduce the accumulation of MyoD, myostatin and atrogin-1 in denervated rat skeletal muscle

机译:拉伸和电刺激减少了失神经的大鼠骨骼肌中MyoD,myostatin和atrogin-1的积累

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摘要

Denervation causes muscle atrophy and incapacity in humans. Although electrical stimulation (ES) and stretching (St) are commonly used in rehabilitation, it is still unclear whether they stimulate or impair muscle recovery and reinnervation. The purpose of this study was to evaluate the effects of ES and St, alone and combined (ES + St), on the expression of genes that regulate muscle mass (MyoD, Runx1, atrogin-1, MuRF1 and myostatin), on muscle fibre cross-sectional area and excitability, and on the expression of the neural cell adhesion molecule (N-CAM) in denervated rat muscle. ES, St and ES + St reduced the accumulation of MyoD, atrogin-1 and MuRF1 and maintained Runx1 and myostatin expressions at normal levels in denervated muscles. None of the physical interventions prevented muscle fibre atrophy or N-CAM expression in denervated muscles. In conclusion, although ES, St and ES + St changed gene expression, they were insufficient to avoid muscle fibre atrophy due to denervation.
机译:去神经引起人类肌肉萎缩和丧失能力。尽管在康复中通常使用电刺激(ES)和伸展运动(St),但仍不清楚它们是否刺激或损害肌肉的恢复和神经支配。这项研究的目的是评估单独和联合使用ES和St(ES + St)对调节肌肉质量的基因(MyoD,Runx1,atrogin-1,MuRF1和myostatin)对肌肉纤维的影响横截面积和兴奋性,以及失神经大鼠肌肉中神经细胞粘附分子(N-CAM)的表达。 ES,St和ES + St减少了失神经肌肉中MyoD,atrogin-1和MuRF1的积累,并使Runx1和myostatin表达保持正常水平。物理干预均不能阻止失神经肌肉的肌纤维萎缩或N-CAM表达。总之,尽管ES,St和ES + St改变了基因表达,但它们不足以避免由于去神经支配而引起的肌纤维萎缩。

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