Abstract
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.
Highlights
The sciatic nerve injury can be caused by incorrect intramuscular injection of medication in the gluteal region in clinic
Peroneus longus muscle atrophy in rats can be improved by EA stimulation of GB30 and ST36 points after sciatic nerve injury induced by penicillin injection
The mechanism of maintaining the normal protein synthesis may be to restore the function of mitochondria and sarcoplasmic reticulum (SR) and upregulate the Glycyl-tRNA synthetase (GlyRS) expression
Summary
The sciatic nerve injury can be caused by incorrect intramuscular injection of medication in the gluteal region in clinic. This is an iatrogenic injury which can be avoided but still exists, especially in developing countries. The injury can lead to lower limb muscle atrophy and even disability. The treatment of muscular atrophy is a global urgent problem because the understanding of muscle atrophy mechanisms is not completely clear. The current understanding of the mechanisms for muscle atrophy is attributed to an increase in protein degradation and/or a decrease in protein synthesis. The increase in protein degradation is mainly due to the activation of the ubiquitin-proteasome pathway, while the information on the mechanism of the protein synthesis reduction is limited [3]
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