| Project/Area Number |
16500341
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Rehabilitation science/Welfare engineering
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| Research Institution | Kobe University |
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Principal Investigator |
SAURA Ryuichi Kobe University, School of Medicine, Associate Professor, 医学部, 助教授 (10252769)
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| Co-Investigator(Kenkyū-buntansha) |
TERASHI Hiroto Kobe University, School of Medicine, Associate Professor, 医学部附属病院, 助教授 (80217421)
SUGIMOTO Masaharu Kobe University, School of Medicine, Associate Professor, 医学部, 助教授 (20379457)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | Ultrasound / Pressure sore / Angiogenesis / Prostaglandin E2 / basic Fibroblast growth factor / Hepatocyte growth factor / Vascular endothelial cell growth factor / real time PCR / 鶏胎芽漿膜血管モデル / 褥瘡 / 肝細胞増殖因子 / 血管内皮細胞増殖因子 / real time PCR |
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| Research Abstract |
Though ultrasound is applied to the treatment of pressure sore, there was little evidence of benefit associated with the use of it in the treatment of pressure sore. Therefore, in order to investigate the therapeutic evidence of ultrasound exposure in the wound healing, the effect of low intensity pulsed-ultrasound on the mRNA induction of COX-1/2 which is the key enzyme for producing prostaglandin E2 (PGE2), basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF) and vascular endothelial cell growth factor (VEGF) in human dermal fibroblasts was examined. Human dermal fibroblasts obtained from skin samples were exposed to a low intensity pulsed-ultrasound by specifically designed apparatus. An enzyme-linked immunosorbent assay determined the release of PGE2 in the medium. Also, mRNA extracted from the cells was reverse-transcribed and amount of cDNA was measured by real-time PCR assay. A low intensity pulsed-ultrasound increases the PGE2 release of dermal fibroblasts in a time-dependent fashion. PGE2 release by 30 mW/cm^2 ultrasound exposure reached maximum 1.24-fold at 1 hour with COX-2 mRNA induction. Also, mRNA induction of basic bFGF,HGF and VEGF were enhanced by a low intensity pulsed-ultrasound exposure for 4 hours. These inductions were supposed to be independent of the PGE2 release by a low intensity pulsed-ultrasound exposure because COX-2 selective inhibitor, NS-398 failed to suppress these inductions of mRNA of angiogenic factor. Thus, our results identify the effect of low intensity pulsed ultrasound to explain the potential mechanism by which it may augment the healing of skin ulcer. Further studies are required to ascertain the direct biological relevance of the low intensity pulsed-ultrasound in angiogenesis, which is required for the tissue development and regeneration.
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