Identification of the control factor of occurrence and prolonged pain of scarring Identification of regulator generation and prolonged pain of scar

疤痕发生及持续疼痛的控制因素识别 疤痕产生及持续疼痛的调节因子识别

• 批准号: 23590725
• 负责人: SUETOMI Katsutoshi
• 金额: $ 2.91万
• 依托单位: Aichi Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23590725/
• 关键词: 瘢痕; 慢性疼痛; マクロファージ; コラーゲン線維; CGRP; ED-1; α-SMA; CGRPの発現; ミエリン鞘の断片化; マイクロアレイ法; 細胞外マトリクス分子; 瘢痕モデル; 疼痛; コラーゲン繊維

The animal model with painful scar was developed in rats and mouse by extensively stripping subcutaneous tissue from the plantar in the hind paw. The mechanical pain threshold decreased specifically in the ipsilateral plantar in animals with scar. This state was maintained for 12 weeks. A collagen layer developed from fibers derma to the muscular layer in the scar tissue in which many fibroblasts were observed. No statistical differences were found for the areas of the c-Fos-immunoreactive (c-Fos-IR) neurons in the ipsilateral and contralateral sides of the L5 level of the dorsal horn in both the Scar group and Pinhole (sham operation) group. However, myelin sheath fragmentation of the nerve fibers was observed in the ipsilateral dorsal root at the L5 position. Similar behavioral findings were observed in mouse models and TNF and Interleukin associate mRNA was increased in ipsilateral DRG.

通过广泛剥离大鼠和小鼠后爪足底皮下组织，建立具有疼痛性瘢痕的动物模型。在有瘢痕的动物中，机械痛阈特别在同侧足底降低。这种状态维持了12周。瘢痕组织中纤维真皮层向肌层发展为胶原层，并可见大量成纤维细胞。瘢痕组和针孔（假手术）组同侧和对侧L5节段背角c-Fos免疫反应（c-Fos-IR）神经元面积差异无统计学意义。然而，在L5位置的同侧背根中观察到神经纤维的髓鞘断裂。在小鼠模型中观察到类似的行为发现，并且在同侧DRG中TNF和白细胞介素相关mRNA增加。