Himori Koichi, Tatebayashi Daisuke, Kanzaki Keita, Wada Masanobu, Westerblad Håkan, Lanner Johanna T, Yamada Takashi
Graduate School of Health Sciences, Sapporo Medical University, Sapporo, Japan.
Faculty of Health and Welfare Science, Okayama Prefectural University, Soja, Okayama, Japan.
PLoS One. 2017 Jun 21;12(6):e0179925. doi: 10.1371/journal.pone.0179925. eCollection 2017.
Skeletal muscle weakness is a prominent feature in patients with rheumatoid arthritis (RA). In this study, we investigated whether neuromuscular electrical stimulation (NMES) training protects against skeletal muscle dysfunction in rats with adjuvant-induced arthritis (AIA). AIA was produced by intraarticular injection of complete Freund's adjuvant into the knees of Wistar rats. For NMES training, dorsiflexor muscles were stimulated via a surface electrode (0.5 ms pulse, 50 Hz, 2 s on/4 s off). NMES training was performed every other day for three weeks and consisted of three sets produced at three min intervals. In each set, the electrical current was set to achieve 60% of the initial maximum isometric torque and the current was progressively increased to maintain this torque; stimulation was stopped when the 60% torque could no longer be maintained. After the intervention period, extensor digitorum longus (EDL) muscles were excised and used for physiological and biochemical analyses. There was a reduction in specific force production (i.e. force per cross-sectional area) in AIA EDL muscles, which was accompanied by aggregation of the myofibrillar proteins actin and desmin. Moreover, the protein expressions of the pro-oxidative enzymes NADPH oxidase, neuronal nitric oxide synthase, p62, and the ratio of the autophagosome marker LC3bII/LC3bI were increased in AIA EDL muscles. NMES training prevented all these AIA-induced alterations. The present data suggest that NMES training prevents AIA-induced skeletal muscle weakness presumably by counteracting the formation of actin and desmin aggregates. Thus, NMES training can be an effective treatment for muscle dysfunction in patients with RA.
骨骼肌无力是类风湿关节炎(RA)患者的一个显著特征。在本研究中,我们调查了神经肌肉电刺激(NMES)训练是否能预防佐剂诱导性关节炎(AIA)大鼠的骨骼肌功能障碍。通过向Wistar大鼠膝关节内注射完全弗氏佐剂来诱导AIA。对于NMES训练,通过表面电极刺激背屈肌(0.5毫秒脉冲,50赫兹,2秒开/4秒关)。NMES训练每隔一天进行一次,持续三周,每次训练由三组组成,每组间隔三分钟。在每组训练中,将电流设置为达到初始最大等长扭矩的60%,并逐渐增加电流以维持该扭矩;当无法再维持60%的扭矩时停止刺激。干预期结束后,切除趾长伸肌(EDL)用于生理和生化分析。AIA大鼠的EDL肌肉中比肌力产生(即每横截面积的力)降低,同时伴有肌原纤维蛋白肌动蛋白和结蛋白的聚集。此外,AIA大鼠的EDL肌肉中促氧化酶NADPH氧化酶、神经元型一氧化氮合酶、p62的蛋白表达以及自噬体标记物LC3bII/LC3bI的比值增加。NMES训练可防止所有这些AIA诱导的改变。目前的数据表明,NMES训练可能通过对抗肌动蛋白和结蛋白聚集体的形成来预防AIA诱导的骨骼肌无力。因此,NMES训练可能是治疗RA患者肌肉功能障碍的一种有效方法。