Tendinopathy is a progressive pathology of tendon that is characteristic of imbalance between matrix synthesis and degeneration and is often caused by failure to adapt to mechanical loading. Non-steroidal anti-inflammatory medications (NSAIDS) are used as a conventional treatment to alleviate pain and swelling in the short term, but the ideal treatment for tendinopathy remains unclear. Here, we show a single pulsed electromagnetic field (SPEMF, 0.2 Hz) that up-regulated tenogenic gene expression (Col1a1, Col3a1, Scx, Dcn) and down-regulated inflammatory gene expression (Mmp1) in vitro. After five days of SPEMF stimulation (3 min/day), the collagen type I and total collagen synthesis protein levels were significantly increased. Under pro-inflammatory cytokine (IL-1β) irritation, the decreased expression of Col1a1/Col3a1 was up-regulated by SPEMF treatment, and the increased expression of Mmp1 was also reversed. From the above, it can be inferred that SPEMF that enhances matrix synthesis and reduces matrix degeneration may counteract the imbalance in tendinopathy. SPEMF application may be developed as a potential future strategy for therapeutic intervention in tendon disorders.

中文翻译：

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单脉冲电磁场​​可增强肌腱细胞中的胶原蛋白合成。

肌腱病是一种肌腱的进行性病理，其特征是基质合成与变性之间的不平衡，通常是由于无法适应机械负荷引起的。非甾体类抗炎药（NSAIDS）作为短期缓解疼痛和肿胀的常规疗法，但肌腱病的理想疗法尚不清楚。在这里，我们显示了一个单脉冲电磁场​​（SPEMF，0.2 Hz），在体外上调肌腱基因表达（Col1a1，Col3a1，Scx，Dcn）和下调炎症基因表达（Mmp1）。在SPEMF刺激五天后（3分钟/天），I型胶原蛋白和总胶原蛋白合成蛋白水平显着增加。在促炎性细胞因子（IL-1β）刺激下，SPEMF处理可上调Col1a1 / Col3a1的表达下降，而Mmp1的表达也被逆转。从以上可以推断，增强基质合成并减少基质变性的SPEMF可以抵消肌腱病的不平衡。SPEMF的应用可能会发展为对肌腱疾病进行治疗干预的潜在未来策略。