Several experimental studies demonstrated that ESWT induces nitric oxide (NO) production and inhibition of nuclear factor kappa B (NF-κB) activation in an in vitro model, and significantly induces the expression of 84 angiogenic genes in normal mice or mice with non-healing diabetic ulcers. With its development, it has been gradually applied in the treatment of musculoskeletal diseases, such as plantar fasciitis and chronic lateral epicondylitis (tennis elbow), for which it is approved by the US Food and Drug Administration. In conclusion, suppressed epithelial-mesenchymal transition might be responsible for the anti-scarring effect of ESWT, and has potential as a therapeutic target in the management of post-burn scars.Įxtracorporeal shockwave therapy (ESWT) is a non-invasive physiotherapy that was first used in the lithotripsy of kidney stones. Expression of inhibitor of DNA binding 1 and 2 was increased. Expression of E-cadherin was increased, while that of N-cadherin was reduced. Transforming growth factor beta 1 (TGF-β1) expression was reduced and alpha smooth muscle actin (α-SMA), collagen-I, fibronectin, and twist-1 were reduced significantly after ESWT.
While HTSF viability was not affected, migration was decreased by ESWT. At 24 h and 72 h after treatment, real-time PCR and western blotting were used to detect mRNA and protein expression, respectively, and cell viability and mobility were assessed.
We cultured primary dermal fibroblasts derived from human HTS and exposed these cells to 1000 impulses of 0.03, 0.1, and 0.3 mJ/mm 2. The objective of this study was to elucidate the mechanism underlying changes in cellular and molecular biology that is induced by ESWT of fibroblasts derived from scar tissue (HTSFs). However, the mechanism underlying the observed beneficial effects is not well understood. Extracorporeal shock wave therapy (ESWT) considerably improves the appearance and symptoms of post-burn hypertrophic scars (HTS).
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