Pharmacological prevention of noise induced hearing loss

在德国，14岁以上的人口中有19%的人有听力障碍。噪声是造成后天性听力损失的主要原因。到目前为止，保守的方法，如听力保护已被用来防止听力损害。目前尚无预防性药物治疗。在这项研究中，活性物质被确定为预防性治疗噪声引起的暂时性（TTS）和永久性（PTS）阈值偏移。由于内耳的压力在生命过程中反复复发，并且创伤随着时间的推移而积累，因此必须长期应用活性物质。一种在内耳中长时间释放活性成分的创新方法是基于细胞的治疗。细胞可以被遗传修饰以过表达生长因子蛋白。在本研究中，这种创新的治疗策略的基础进行了调查。选择的生长因子胶质细胞源性神经营养因子，促红细胞生成素和胰岛素样生长因子-1检查其保护听力免受噪声创伤的潜力。在相应的动物模型中，检查创伤暴露前后的声阈值，并与未治疗动物的声阈值进行比较。

In Germany, 19 % of the population aged older than 14 years are hearing impaired. Noise is said to be the main reason for avoidable acquired hearing loss. To date, conservative methods such as hearing protection have been used to prevent hearing impairment. No preventive pharmacological therapies are available. In this study, active substances are identified for the preventive treatment of noise induced temporary (TTS) and permanent (PTS) threshold shift. As the stress on the inner ear repeatedly recurs within the course of life, and the traumas accumulate over time, a long-term application of the active substances is mandatory. An innovative way to release active ingredients over an extended period of time in the inner ear is cell-based therapy. Cells can genetically be modified to overexpress growth factor proteins. In the present study the basis for this innovative therapy strategy is investigated. The selected growth factors glial cell line-derived neurotrophic factor, erythropoietin and insulin-like growth factor-1 are examined for their potential to protect the hearing from noise trauma. In corresponding animal models, the acoustic thresholds before and after trauma exposure are examined and compared with those of non-treated animals.