Department of Otorhinolaryngology and Head and Neck Surgery, Ernst Moritz Arndt University, Walther Rathenau Str 43-45, 17475 Greifswald, Germany.
Eur Arch Otorhinolaryngol. 2012 Jan;269(1):87-92. doi: 10.1007/s00405-011-1627-6. Epub 2011 May 18.
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.
需要建立一种慢性鼓膜穿孔的动物模型，以便进行促进鼓膜穿孔愈合的实验。碱性成纤维细胞生长因子在鼓膜创伤愈合中起着重要作用。本研究的目的是观察成纤维细胞生长因子受体 1（FGFR1）抑制对实验性鼓膜穿孔愈合的疗效。在 12 只大鼠双侧进行器械性鼓膜切开术。将 FGFR1 酪氨酸激酶的一种特异性抑制剂（SU5402）以每日 2mg/ml 剂量应用于左侧鼓膜（2mg/ml），以 10mg/ml 剂量应用于右侧鼓膜，连续 12 天。此后，每周观察鼓膜愈合情况，共 30 天。鼓膜愈合呈剂量依赖性延迟。我们观察到两组之间的组织学参数存在差异。SU5402 是一种强有力的鼓膜愈合抑制剂，但似乎不适合在大鼠中建立慢性鼓膜穿孔。
