首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Effect of Electroacupuncture on the Expression of Glycyl-tRNA Synthetase and Ultrastructure Changes in Atrophied Rat Peroneus Longus Muscle Induced by Sciatic Nerve Injection Injury
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Effect of Electroacupuncture on the Expression of Glycyl-tRNA Synthetase and Ultrastructure Changes in Atrophied Rat Peroneus Longus Muscle Induced by Sciatic Nerve Injection Injury

机译:电针对坐骨神经注射致萎缩大鼠腓骨长肌糖基-tRNA合成酶表达及超微结构的影响。

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摘要

Glycyl-tRNA synthetase (GlyRS) is one of the key enzymes involved in protein synthesis. Its mutations have been reported to cause Charcot-Marie-Tooth disease which demonstrates muscular atrophy in distal extremities, particularly manifested in peroneus muscles. In this situation, the dysfunctions of mitochondria and sarcoplasmic reticulum (SR) affect energy supply and excitation-contraction coupling of muscle fibers, therefore resulting in muscular atrophy. Although the treatment of muscular atrophy is a global urgent problem, it can be improved by electroacupuncture (EA) treatment. To investigate the mechanism underlying EA treatment improving muscular atrophy, we focused on the perspective of protein synthesis by establishing a penicillin injection-induced sciatic nerve injury model. In our model, injured rats without treatment showed decreased sciatic functional index (SFI), decreased peroneus longus muscle weight and muscle fiber cross-sectional area, aggregated mitochondria with vacuoles appearing, swollen SR, and downregulated mRNA and protein expression levels of GlyRS and myosin heavy chain IIb (MHC-IIb). The injured rats with EA treatment showed significant recovery. These results indicated that EA stimulation can alleviate peroneus longus muscular atrophy induced by iatrogenic sciatic nerve injury through promoting the recovery of GlyRS and muscle ultrastructure and increasing muscle protein synthesis.
机译:糖基-tRNA合成酶(GlyRS)是参与蛋白质合成的关键酶之一。据报道,其突变导致夏科特-玛丽齿病,该病表现出末梢肌肉萎缩,特别是在腓骨肌肉中。在这种情况下,线粒体和肌质网(SR)的功能障碍会影响能量供应和肌肉纤维的兴奋-收缩耦合,从而导致肌肉萎缩。尽管肌肉萎缩症的治疗是全球性的紧迫问题,但可以通过电针(EA)治疗加以改善。为了研究EA治疗改善肌肉萎缩的潜在机制,我们通过建立青霉素注射液诱导的坐骨神经损伤模型,着眼于蛋白质合成的观点。在我们的模型中,未经治疗的受伤大鼠表现出坐骨神经功能指数(SFI)降低,腓骨长肌重量和肌纤维横截面积降低,线粒体聚集,液泡出现,SR肿胀以及GlyRS和肌球蛋白的mRNA和蛋白表达水平下调重链IIb(MHC-IIb)。接受EA治疗的受伤大鼠显示出明显的恢复。这些结果表明,EA刺激可以通过促进GlyRS的恢复和肌肉超微结构以及增加肌肉蛋白的合成来减轻医源性坐骨神经损伤引起的腓骨长肌萎缩。

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