Background Therapeutic ultrasound (TUS) has been proposed as a potential strategy to accelerate proliferation and regeneration to the damaged tissue. However, the underline mechanism remains modest clarified. The purpose of this study was to determine the mechanism of TUS on ischemia-induced angiogenesis using mice model of hindlimb ischemia.
Methods and results Hindlimb ischemia was induced by unilateral femoral artery resection using 8–12 week-old male C57BL6 mice. External TUS (1.0 MHz, 0.3W/cm2) was then performed for 9 min/day. At postoperative day 14, decreased prevalence of gangrene, increased capillary density and skin temperature ratio between ischaemic/normal extremities were observed in TUS-treated mice. Moreover, the levels of nitric oxide (NO) expression, endothelial nitric oxide synthase (eNOS) and Akt phosphorylation contained in the ischaemic muscles were increased in response to TUS. In vitro, TUS interrupted the process of hypoxia-induced apoptosis and contributed to the tube-formative and proliferative capacities of human umbilical vein endothelial cells. TUS increased the level of NO in the conditioned media, as well as the eNOS and Akt phosphorylation in the cell lysate. Finally, administration of PI3K inhibitor LY294002 and NG-Nitro-L-arginine Methyl Ester (L-NAME) could block these TUS-mediated angiogenic benefits.
Conclusions In conclusion, the present study indicates that external ultrasound exposure contributes to ischemia-induced neovascularization through promoting endothelial functions via Akt-eNOS signal pathway.
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