Extracorporeal Shock Wave Therapy Induces Therapeutic Lymphangiogenesis in a Rat Model of Secondary Lymphoedema

Serizawa, Fukashi; Ito, Kei; Matsubara, Mitsunobu; Sato, Akira; Shimokawa, Hiroaki; Satoh, Susumu

doi:10.1016/j.ejvs.2011.02.029

Cited by 63 publications

(49 citation statements)

References 36 publications

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“…[12] Low-energy ESWT induces therapeutic lymphangiogenesis by up-regulating vascular endothelial growth factor C and basis fibroblast growth factor, and by improving lymphedema in a rat model. [18] So we demonstrate that improvement of post-mastectomy lymphedema occurred due to lymphangiogenesis. Serizawa et al created a rat tail model of lymphedema and subsequently subjected the animals to serial ECT therapy.…”

Section: Discussionmentioning

confidence: 82%

“…Enhanced drainage of lymphaticfluid as well as up-regulation of VEGF-C expression was found in the treatment group compared to the controls. [18] Study was designed to employ established methods to analyze shockwave-induced lymphangiogenesis in vitro. We show that shockwaves alter the biological properties of LEC in terms of proliferation, migration, morphology, marker profiles and gene expression.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have demonstrated the effect of shockwave on the angiogenesis and suppression of the inflammation [13]. ESWT stimulates the lymph-angiogenesis by regulation the vascular endothelial growth factor and basic fibroblast growth factor [14].…”

Section: Introductionmentioning

confidence: 99%

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Response of Post-Mastectomy Lymphedema to Extracorporeal Shockwave Therapy

Elshazly¹,

Borhan²,

Thabet³

et al. 2016

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Introduction: Post-mastectomy lymphedema is a chronic, debilitating disorder that is frequently misdiagnosed, treated too late or not treated at all, Lymphedema (LE) is an abnormal accumulation of protein-rich fluid in the interstitium leading to limb swelling, chronic inflammation and reactive fibrosis of the affected tissues resulting from damage to lymphatic circulation following surgery, chemotherapy and/or radiation therapy. The aim was to investigate the effect of shockwave therapy on the post-mastectomy lymphedema. Subjects and methods: Sixty female patients underwent modified radical mastectomy surgery or lumpectomy, chemotherapy and radiotherapy associated with unilateral lymphedema (stage 2, 3), into two equal groups; their ages ranged from 30-50 years. The study group received shockwave therapy 2 times/week for 6 weeks plus traditional physical therapy program (manual lymphatic drainage, circulatory exercises with elevation, shoulder ROM exercises and pneumatic compression therapy) 3times /week /6weeks. Control group received traditional physical therapy program (manual lymphatic drainage, circulatory exercises with elevation, shoulder ROM exercises and pneumatic compression therapy) 3times /week /6weeks. Evaluation procedures were carried out to measure the upper limb volume measurement, ROM of shoulder flexion, abduction and external rotation. Results: Post treatment results showed that there was a significant improvement difference in shoulder ROM and upper limb volume in both groups in favor of the study group.

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

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Response of Post-Mastectomy Lymphedema to Extracorporeal Shockwave Therapy

Elshazly¹,

Borhan²,

Thabet³

et al. 2016

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“…1A). Based on our previous studies, 15,20,[22][23][24]28,37,39,49,50,54 the shock wave was applied to two spots on the injured spinal cord 3 times a week for 3 weeks after SCI. The treatment was performed immediately after wound closure following SCI, as well as 2, 4, 7, 9, 11, 14, 16, and 18 days after injury.…”

Section: Low-energy Eswtmentioning

confidence: 99%

Low-energy extracorporeal shock wave therapy promotes vascular endothelial growth factor expression and improves locomotor recovery after spinal cord injury

Yamaya¹,

Ozawa²,

Kanno³

et al. 2014

JNS

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Object Extracorporeal shock wave therapy (ESWT) is widely used for the clinical treatment of various human diseases. Recent studies have demonstrated that low-energy ESWT upregulates the expression of vascular endothelial growth factor (VEGF) and promotes angiogenesis and functional recovery in myocardial infarction and peripheral artery disease. Many previous reports suggested that VEGF produces a neuroprotective effect to reduce secondary neural tissue damage after spinal cord injury (SCI). The purpose of the present study was to investigate whether lowenergy ESWT promotes VEGF expression and neuroprotection and improves locomotor recovery after SCI. Methods Sixty adult female Sprague-Dawley rats were randomly divided into 4 groups: sham group (laminectomy only), sham-SW group (low-energy ESWT applied after laminectomy), SCI group (SCI only), and SCI-SW group (low-energy ESWT applied after SCI). Thoracic spinal cord contusion injury was inflicted using an impactor. Low-energy ESWT was applied to the injured spinal cord 3 times a week for 3 weeks. Locomotor function was evaluated using the Basso, Beattie, and Bresnahan (BBB) Scale (open field locomotor score) at different time points over 42 days after SCI. Hematoxylin and eosin staining was performed to assess neural tissue damage in the spinal cord. Neuronal loss was investigated by immunostaining for NeuN. The mRNA expressions of VEGF and its receptor, Flt-1, in the spinal cord were assessed using real-time polymerase chain reaction. Immunostaining for VEGF was performed to evaluate VEGF protein expression in the spinal cord. Results In both the sham and sham-SW groups, no animals showed locomotor impairment on BBB scoring. Histological analysis of H & E and NeuN stainings in the sham-SW group confirmed that no neural tissue damage was induced by the low-energy ESWT. Importantly, animals in the SCI-SW group demonstrated significantly better locomotor improvement than those in the SCI group at 7, 35, and 42 days after injury (p < 0.05). The number of NeuN-positive cells in the SCI-SW group was significantly higher than that in the SCI group at 42 days after injury (p < 0.05). In addition, mRNA expressions of VEGF and Flt-1 were significantly increased in the SCI-SW group compared with the SCI group at 7 days after injury (p < 0.05). The expression of VEGF protein in the SCI-SW group was significantly higher than that in the SCI group at 7 days (p < 0.01). Conclusions The present study showed that low-energy ESWT significantly increased expressions of VEGF and Flt-1 in the spinal cord without any detrimental effect. Furthermore, it significantly reduced neuronal loss in damaged neural tissue and improved locomotor function after SCI. These results suggested that low-energy ESWT enhances the neuroprotective effect of VEGF in reducing secondary injury and leads to better locomotor recovery following SCI. This study provides the first evidence that low-energy ESWT can be a safe and promising therapeutic strategy for SCI.

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“…The primer sequences were as follows: VEGF-C sense, 5′-GCC AAT CAC ACT TCC TGC CG-3′, and VEGF-C antisense, 5′-GTG ATG TAG TAG CTG CAT GAT CG-3′; GAPDH sense, 5′-GTG AGG TGA CCG CAT CTT CT-3′, and GAPDH antisense, 5′-TGG AAG ATG GTG ATG GGT TT-3′. 4,7,14) Griess Assay Detection of NO release was measured in the culture medium using the colorimetric Griess assay. Nitrite, a stable end product of NO, accumulation was determined by mixing equal volumes of cell culture medium and Griess reagent (1% sulfanilamide, 0.1% naphthylethylenediamine, and 5% H 3 PO 4 ).…”

Section: Real-time Polymerase Chain Reaction (Pcr)mentioning

confidence: 99%

Chrysin Inhibits Lymphangiogenesis <i>in Vitro</i>

Prangsaengtong

Athikomkulchai

et al. 2016

Biological & Pharmaceutical Bulletin

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The induction of lymphangiogenesis is an important process to promote cancer growth and cancer metastasis via the lymphatic system. Identifying the compounds that can prevent lymphangiogenesis for cancer therapy is urgently required. Chrysin, 5,7-dihydroxyflavone, a natural flavone extracted from Thai propolis, was used to investigate the effect on the lymphangiogenesis process of TR-LE, rat lymphatic endothelial cells. In this study, maximal nontoxic doses of chrysin on TR-LE cells were selected by performing a proliferation assay. The process of lymphangiogenesis in vitro was determined by cord formation assay, adhesion assay and migration assay. Chrysin at a nontoxic dose (25 μM) significantly inhibited cord formation, cell adhesion and migration of TR-LE cells when compared with the control group. We also found that chrysin significantly induced vascular endothelial growth factor C (VEGF-C) mRNA expression and nitric oxide (NO) production in TR-LE cells which was involved in decreasing the cord formation of TR-LE cells. In conclusion, we report for the first time that chrysin inhibited the process of lymphangiogenesis in an in vitro model. This finding may prove to be a natural compound for anti-lymphangiogenesis that could be developed for use in cancer therapy.

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Extracorporeal Shock Wave Therapy Induces Therapeutic Lymphangiogenesis in a Rat Model of Secondary Lymphoedema

Abstract: The low-energy SW therapy induces therapeutic lymphangiogenesis by up-regulating VEGF-C and bFGF, and improves lymphoedema in a rat-tail model, suggesting that low-energy SW therapy could be a non-invasive and effective strategy for lymphoedema in humans.

Cited by 63 publications

References 36 publications

Response of Post-Mastectomy Lymphedema to Extracorporeal Shockwave Therapy

Response of Post-Mastectomy Lymphedema to Extracorporeal Shockwave Therapy

Low-energy extracorporeal shock wave therapy promotes vascular endothelial growth factor expression and improves locomotor recovery after spinal cord injury

Chrysin Inhibits Lymphangiogenesis <i>in Vitro</i>

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