Effects of Shock Waves on Tenocyte Proliferation and Extracellular Matrix Metabolism
- 作者：Yuan-Hung Chao ; Yang-Hwei Tsuang ; Jui-Sheng Sun ; Li-Ting Chen ; Yueh-Feng Chiang ; Chien-Che Wang ; Ming-Hong Chen
- 关键词：Shock waves ; Tenocytes ; Proliferation ; Collagen ; Nitric oxide
- 刊名：Ultrasound in Medicine and Biology
- 出版年：2008
- 期刊代码：82_03015629
- 类别：ph
- 出版时间：May 2008
- 卷：34
- 期：5
- 页码：841-852
- 文件大小：408 K
摘要
The shock wave is an effective noninvasive modality for resolving various tendon pathologies. However, scientific rationale and mechanism of shock wave therapy remains limited. This study aims to investigate the effects of shock waves and their biochemical mechanisms on tenocyte proliferation and collagen synthesis. Tenocytes harvested from Achilles tendons of Sprague-Dawley rats were used in this study. Cell viability was assayed by trypan blue exclusion methods. The colorimetric assay was determined to evaluate the mitochondria activity of the tenocytes after shock wave exposure. Synthesis of collagen, nitric oxide (NO) and transforming growth factor-β1 (TGF-β1) were determined and their gene expression was also studied. The results showed that there was a dose-dependent impairment of cell viability observed in 0.36 mJ/mm2 and 0.68 mJ/mm2 stimulation. In the proliferation assay, low energy level with low impulses (0.36 mJ/mm2 with 50 and 100 impulses) showed positive stimulatory effects, whereas the high energy level with high impulses (0.68 mJ/mm2 with 250 and 500 impulses) had significant inhibitory effects. At 0.36 mJ/mm2, 100 impulse shock waves treatment, up-regulation of proliferating cell nuclear antigen (PCNA) (at 6 and 24 h) and collagen type I, collagen type III and TGF-β1 gene expression (at 24 h) were observed; these were followed by the increases in NO production (at 24 h), TGF-β1 release (at 48 and 96 h) and collagen synthesis (at the 7th day). This study revealed that shock waves can stimulate tenocyte proliferation and collagen synthesis. The associated tenocyte proliferation is mediated by early up-regulation of PCNA and TGF-β1 gene expression, endogenous NO release and synthesis and TGF-β1 protein and then collagen synthesis. (E-mail: jssun@ym.edu.tw)