Low-energy extracorporeal shock wave therapy enhances skin wound healing in diabetic mice: A critical role of endothelial nitric oxide synthase
Low-energy extracorporeal shock wave therapy enhances skin wound healing in diabetic mice: A critical role of endothelial nitric oxide synthase
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DOI：
10.1111/j.1524-475x.2012.00851.x
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发表时间：
2012-11-01
影响因子：
2.9
通讯作者：
Tachi, Masahiro
中科院分区：
文献类型：
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作者：
Hayashi, Denso;Kawakami, Kazuyoshi;Tachi, Masahiro
低能量体外冲击波（LE-ESW）治疗已被证明可以加速伤口修复；然而，治疗机制仍不清楚。在本研究中，我们探讨了内皮一氧化氮合酶（eNOS）的作用。一次 LE-ESW 治疗加速了糖尿病小鼠注射链脲佐菌素引起的伤口的愈合。这种加速愈合伴随着 eNOS 和血管内皮生长因子 (VEGF) 表达的增加以及伤口组织中新血管的生成。这些结果提出了 eNOS 可能参与 LE-ESW 治疗的有益作用的可能性。为了解决这种可能性，我们比较了 eNOS 基因敲除小鼠（eNOS-KO 小鼠）和野生型（WT）对照小鼠的这种治疗效果。有趣的是，与 WT 小鼠相比，eNOS-KO 小鼠中 LE-ESW 诱导的伤口闭合加速以及 VEGF 表达和新血管形成的增加显着减弱。综合考虑，这些结果表明，LE-ESW 治疗在伤口组织中诱导了 eNOS，并通过促进 VEGF 表达和新血管形成来加速伤口愈合，从而在该治疗的治疗效果中发挥着关键作用。
Low-energy extracorporeal shock wave (LE-ESW) treatment has been shown to accelerate wound repair; however, the mechanisms of treatment remain unclear. In the present study, we addressed the role of endothelial nitric oxide synthase (eNOS). A single LE-ESW treatment accelerated the healing of wounds in diabetic mice caused by the injection of streptozotocin. This accelerated healing was accompanied by the increased expression of eNOS and vascular endothelial growth factor (VEGF) and the generation of new vessels at the wound tissues. These results raised the possibility that eNOS may be involved in the beneficial effects of LE-ESW treatment. To address this possibility, we compared the effects of this treatment between mice with a genetic disruption of eNOS knockout (eNOS-KO mice) and wild-type (WT) control mice. Interestingly, the LE-ESW-induced acceleration of wound closure and the increase in VEGF expression and neovascularization was significantly attenuated in eNOS-KO mice compared with WT mice. Considered collectively, these results showed that eNOS was induced at the wound tissues by LE-ESW treatment and played a critical role in the therapeutic effects of this treatment by accelerating the wound healing by promoting VEGF expression and neovascularization.