title: Electrical stimulation by semi-implantable electrodes decreases the levels of proteins associated with sciatic nerve injury-induced muscle atrophy.
abstract: Muscle atrophy is a disease that is usually caused by denervation. The aim of the present study was to determine whether electrical stimulation by semi-implantable electrodes is capable of decreasing the levels of specific proteins associated with sciatic nerve injury-induced muscle atrophy. Male Sprague Dawley (SD) rats with damaged sciatic nerves were maintained on a 12‑h light/dark cycle. Thirty-two SD rats were randomly allocated into 4 groups (each group, n=8). The rats in group C received no electrical stimulation; the rats in groups D, N and DN received electrical stimulation by semi-implantable electrodes during the daytime alone, nighttime alone and both the daytime and nighttime, respectively. Immunoblot assays were performed to detect the expression of cellular proteins associated with muscle atrophy. The number of muscle satellite cells was determined using a microscope, indicating that electrical stimulation increased the number of muscle satellite cells. Immunoblot assay results showed that electrical stimulation reduced the expression levels of cathepsin L, calpain 1 and the ubiquitinated muscle ring finger‑1 (MuRF-1) protein. In conclusion, electrical stimulation by semi-implantable electrodes constitutes a potential method for the treatment of sciatic nerve injury-induced muscle atrophy. The decreased expression levels of the cellular proteins cathepsin L and calpain 1, as well as the ubiquitinated protein MuRF-1, are associated with the attenuation of sciatic nerve injury-induced muscle atrophy.
authors.affiliation: Department of Hand Surgery, the Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, PR China. liujun88665@163.com
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
authors.forename: Kuangwen
authors.initials: K
authors.lastname: Li
authors.forename: Xiongjie
authors.initials: X
authors.lastname: Huang
authors.forename: Junfeng
authors.initials: J
authors.lastname: Xie
authors.forename: Xinfeng
authors.initials: X
authors.lastname: Huang
mesh_terms: D000818:Animals; D001835:Body Weight; D002154:Calpain / Q000378:metabolism; D056668:Cathepsin L / Q000378:metabolism; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D008297:Male; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000294:innervation / Q000473:pathology; D009133:Muscular Atrophy / Q000209:etiology / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D009929:Organ Size; D059348:Peripheral Nerve Injuries / Q000628:therapy*; D051381:Rats; D032496:Satellite Cells, Skeletal Muscle / Q000166:cytology; D020426:Sciatic Neuropathy / Q000628:therapy*; D000070584:Tripartite Motif Proteins; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism; D057149:Ubiquitinated Proteins / Q000378:metabolism
chemical_list: D009124:Muscle Proteins; D000070584:Tripartite Motif Proteins; D057149:Ubiquitinated Proteins; C440908:TRIM63 protein, human; D044767:Ubiquitin-Protein Ligases; D002154:Calpain; D056668:Cathepsin L