Sun Lijun, Sun Shuxin, Zhao Xinjuan, Zhang Jing, Guo Jianzhong, Tang Liang, Ta Dean
Institute of Sports Biology, Shaanxi Normal University, Xi'an, 710119, China.
Department of Electronic Engineering, Fudan University, Shanghai, 200433, China.
J Med Ultrason (2001). 2019 Oct;46(4):377-388. doi: 10.1007/s10396-019-00962-2. Epub 2019 Aug 3.
Low-intensity pulsed ultrasound (LIPUS) is effective in promoting bone healing, and a myostatin deficiency also has a positive effect on bone formation. In this study, we evaluated the effects of LIPUS on bone healing in rats in vivo and investigated the mechanisms in vitro, aiming to explore whether LIPUS promotes bone healing through inhibition of the myostatin signaling pathway.
Rats with both drill-hole defects and MC3T3-E1 cells were randomly assigned to a LIPUS group and a control group. The LIPUS group received LIPUS treatment (1.5 MHz, 30 mW/cm) for 20 min/day.
After 21 days, the myostatin expression in quadriceps was significantly inhibited in the LIPUS group, and remodeling of the newly formed bone in the drill-hole site was significantly better in the LIPUS group than that in the control group, which was confirmed by micro-CT analysis. After 3 days, LIPUS significantly promoted osteoblast proliferation; inhibited the expression of AcvrIIB (the myostatin receptor), Smad3, p-Smad3, and GSK-3β; and increased Wnt1 and β-catenin expression. Moreover, translocation of β-catenin from the cytolemma to the nucleus was observed in the LIPUS group. However, these effects were blocked by treatment with myostatin recombinant protein.
The results indicate that LIPUS may promote bone healing through inhibition of the myostatin signal pathway.
低强度脉冲超声（LIPUS）可有效促进骨愈合，而肌生成抑制素缺乏对骨形成也有积极作用。在本研究中，我们评估了LIPUS对大鼠体内骨愈合的影响，并在体外研究其机制，旨在探讨LIPUS是否通过抑制肌生成抑制素信号通路促进骨愈合。
将有钻孔缺损的大鼠和MC3T3-E1细胞随机分为LIPUS组和对照组。LIPUS组接受LIPUS治疗（1.5MHz，30mW/cm²），每天20分钟。
21天后，LIPUS组股四头肌中肌生成抑制素的表达明显受到抑制，微CT分析证实，LIPUS组钻孔部位新形成骨的重塑明显优于对照组。3天后，LIPUS显著促进成骨细胞增殖；抑制AcvrIIB（肌生成抑制素受体）、Smad3、p-Smad3和GSK-3β的表达；并增加Wnt1和β-连环蛋白的表达。此外，在LIPUS组中观察到β-连环蛋白从细胞膜向细胞核的转位。然而，用肌生成抑制素重组蛋白处理可阻断这些作用。
结果表明，LIPUS可能通过抑制肌生成抑制素信号通路促进骨愈合。
