Wang Meng, Zhang Xiao Ming, Yang Sheng Bo
Department of Anatomy, Zunyi Medical College, Zunyi, Guizhou 563000, China.
Department of Anatomy, Zunyi Medical College, Zunyi, Guizhou 563000, China; Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Evid Based Complement Alternat Med. 2016;2016:7536234. doi: 10.1155/2016/7536234. Epub 2016 May 4.
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.
甘氨酰 - tRNA合成酶(GlyRS)是参与蛋白质合成的关键酶之一。据报道,其突变会导致夏科 - 马里 - 图斯病,该病表现为远端肢体肌肉萎缩,尤其在腓骨肌中表现明显。在这种情况下,线粒体和肌浆网(SR)的功能障碍会影响肌纤维的能量供应和兴奋 - 收缩偶联,从而导致肌肉萎缩。尽管肌肉萎缩的治疗是一个全球性的紧迫问题,但电针(EA)治疗可以改善这种情况。为了研究EA治疗改善肌肉萎缩的机制,我们通过建立青霉素注射诱导的坐骨神经损伤模型,从蛋白质合成的角度进行了研究。在我们的模型中,未经治疗的损伤大鼠坐骨神经功能指数(SFI)降低,腓骨长肌重量和肌纤维横截面积减小,线粒体聚集并出现空泡,SR肿胀,GlyRS和肌球蛋白重链IIb(MHC - IIb)的mRNA和蛋白质表达水平下调。接受EA治疗的损伤大鼠显示出明显的恢复。这些结果表明,EA刺激可通过促进GlyRS和肌肉超微结构的恢复以及增加肌肉蛋白质合成,减轻医源性坐骨神经损伤诱导的腓骨长肌萎缩。