Inhibition of fibroblast growth factor receptor 1: influence on tympanic membrane wound healing in rats

被引：14
作者：
Kaftan, Holger [1 ,2 ]
Reuther, Lars [2 ]
Miehe, Baerbel [3 ]
Hosemann, Werner [2 ]
Beule, Achim [2 ]
机构：
[1] Ernst Moritz Arndt Univ Greifswald, Dept Otorhinolaryngol & Head & Neck Surg, D-17475 Greifswald, Germany
[2] Ernst Moritz Arndt Univ Greifswald, Dept Otorhinolaryngol & Head & Neck Surg, D-17475 Greifswald, Germany
[3] Ernst Moritz Arndt Univ Greifswald, Dept Anat & Cell Biol, D-17489 Greifswald, Germany
来源：
EUROPEAN ARCHIVES OF OTO-RHINO-LARYNGOLOGY | 2012年 / 269卷 / 01期
关键词：
FGFR; 1; SU5402; Tympanic membrane; Myringotomy; Wound healing; TOPICAL APPLICATION; ANIMAL-MODEL; PERFORATIONS; CONTRIBUTES;
D O I：
10.1007/s00405-011-1627-6
中图分类号：
R76 [耳鼻咽喉科学];
学科分类号：
100213 ;
摘要：
An animal model of chronic tympanic membrane (TM) perforation is needed for experiments on supporting healing of TM perforations. The basic fibroblast growth factor is important in TM wound healing. The object of this study was to investigate the efficacy of fibroblast growth factor receptor 1 (FGFR1) inhibition to arrest wound healing of experimental TM perforation. Bilateral instrumental myringotomies were performed in 12 rats. A specific inhibitor of the FGFR1 tyrosine kinase (SU5402) was applied to the left TM (2 mg/ml) and to the right TM (10 mg/ml) of each animal daily for 12 consecutive days. Thereafter, TMs were observed weekly for a total of 30 days. TM healing was delayed in a dose-dependent manner. We observed differences in the histologic parameters between both groups. SU 5402 is a strong inhibitor of TM healing but seems not to be suitable to create a chronic TM perforation in rat.
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收藏
页码：87 / 92
页数：6
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