Basic research of factors affecting the formation of granulation tissue in wound healing.

影响伤口愈合肉芽组织形成因素的基础研究。

• 批准号: 11671789
• 负责人: TAOHI Masahiro
• 金额: $ 2.18万
• 依托单位: Teikyo University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2001
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671789/
• 关键词: wound healing; pressure uclcers; hypertrophic scar; keloid; 創傷治療; 神経伝達物質; 動物モデル; db; dbマウス; 血管新生

1. Intraperitoneal and oral administration of Piracetam accelerated wound healing in rats. In both incisional wounds and open wounds, piracetam raised wound breaking strength.2. S- 1452 ; thromboxane A2 blockade, did not show any beneficial effects of rat wound healing. The failure of this study would be attributed to the antiplatelet actions.3. We examined a simple experimental model in the rat and investigated the mechanism of formation of pressure ulcers. We planned three patterns of ischemia-reperfusion procedure. In each pattern the pressure of the treated site and total time of ischemia was same. Monitoring the skin blood flow, reactive hyperemia was not seen in one pattern. One week after experiment, in two patterns, skin necrosis of the treated sites were recognized. By this experiment, it is suggested that the formation of pressure ulcers is not dependent upon only the total pressure but also the patterns of pressure.4. We estimated the efficacy of keloid implantation to nude mouse and creating hypertrophic scar in the rabbit ears. The implanted keloid disappeared rapidly. The rabbit ear wound were got hypertrophic with cauterized the wound margin. So the delay of epithelization has the key role for keloid formation.5. The expression of markers of epidermal proliferation and differentiation was assessed immunohistologically in hypertrophic scar tissue and site-matched controls from the same patients. The epidermis appeared thicker in all-hypertrophic scars when comparing with controls. Staining for Ki-67 antigen revealed an increase in hypertrophic scar basal cells in twelve cases out of fourteen cases. No difference in the expression of differentiation markers was observed between hypertrophic scars and controls.Our results raise the" possibility that acanthosis in hypertrophic scar represents a feature, which is shared with tissue expansion and, a number of conditions with the epidermis covering proliferative dermal tumors.

1.吡拉西坦腹腔和口服给药促进大鼠伤口愈合。在切口和开放性伤口中，吡拉西坦均能提高伤口的断裂强度. S- 1452 ;血栓烷A2阻断剂，未显示对大鼠伤口愈合的任何有益作用。本研究的失败可能与抗血小板作用有关.我们研究了一个简单的实验模型，在大鼠和调查的机制形成的压力溃疡。我们设计了三种缺血再灌注程序模式。每种模式治疗部位的压力和总缺血时间相同。监测皮肤血流，在一种模式中未观察到反应性充血。实验后一周，在两种模式中，治疗部位的皮肤坏死被识别。提示压疮的形成不仅取决于总压力，还取决于压力模式.我们评估了瘢痕疙瘩植入裸小鼠并在兔耳中形成增生性瘢痕的疗效。植入的瘢痕疙瘩迅速消失。烧灼兔耳创面，使创面增生。因此，上皮化延迟是瘢痕疙瘩形成的关键.在同一患者的增生性瘢痕组织和位点匹配的对照中，对表皮增殖和分化标志物的表达进行免疫组织学评估。与对照组相比，所有增生性瘢痕的表皮均较厚。Ki-67抗原染色显示14例中有12例增生性瘢痕基底细胞增多。在增生性瘢痕和对照组之间没有观察到分化标志物的表达差异。我们的结果提出了增生性瘢痕中棘皮症代表一种特征的可能性，这种特征与组织扩张以及表皮覆盖增生性真皮肿瘤的一些情况是共享的。

项目成果

館 正弘: "トロンボキサンA2受容体拮抗剤は創傷治癒促進作用はない"Progress in Medicine. 20. 2332-2334 (2000)

Masahiro Tate：“血栓素 A2 受体拮抗剂对促进伤口愈合没有作用”医学进展 20. 2332-2334 (2000)。

Masahiro Tachi: "The animal models for wound healing and dermatitis, in Analysis of skin mechanisms"Takausu Kasuhiro ed. Gijutu-Johou Kyoukai. 165-182 (1999)

Masahiro Tachi：“伤口愈合和皮炎的动物模型，皮肤机制分析”Takausu Kasuhiro 编辑。