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首页> 外文期刊>The Laryngoscope: A Medical Journal for Clinical and Research Contributions in Otolaryngology, Head and Neck Medicine and Surgery, Facial Plastic and Reconstructive Surgery .. >Pharmacological protection of hearing loss in the mouse model of endolymphatic hydrops.
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Pharmacological protection of hearing loss in the mouse model of endolymphatic hydrops.

机译：内淋巴积水小鼠模型中听力损失的药理保护。

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OBJECTIVES/HYPOTHESIS: Excitotoxic and related inflammatory injury are implicated in the spiral ganglion degeneration seen with Meniere's disease and endolymphatic hydrops (ELH). Excitotoxicity is initiated with glutamate elevation and associated with downstream increases in reactive oxygen species resulting in inflammation-mediated neuronal degeneration. This study tests the hypothesis that interruption of the initial and/or downstream aspects of excitotoxicity should provide hearing protection in ELH-associated hearing loss. STUDY DESIGN: This study tests whether riluzole, a glutamate release inhibitor, and dimethylsulfoxide (DMSO), an anti-inflammatory and antioxidant solvent with favorable properties at the level of glutamate receptors, can protect against early-stage hearing loss in a mouse model of ELH. METHODS: The Phex(Hyp-Duk) mouse spontaneously develops ELH and postnatal hearing loss. Starting at postnatal day 6 (P6), daily injections of riluzole + DMSO or just DMSO were administered. Untreated mutants served as controls. At P21, P25, and P30, hearing function was assessed by recording auditory brainstem responses. A cochlear function index was developed to assess global cochlear function at each time point. RESULTS: Compared to no treatment, DMSO provided significant hearing protection (P < .05). The riluzole + DMSO also showed protection, but it was statistically indistinguishable from DMSO alone; a synergistic increase in protection with riluzole was not observed. CONCLUSIONS: This study demonstrates pharmacological hearing protection in an animal model of ELH. The results support the assertion that inflammatory (reactive oxygen species) injury, which is part of the excitotoxic pathway, contributes to the development of ELH-associated hearing loss.
机译：目的/假设：兴奋性毒性和相关的炎性损伤与梅尼埃病和内淋巴积水（ELH）所致的螺旋神经节变性有关。兴奋性毒性由谷氨酸升高引起，并与下游活性氧增加有关，导致炎症介导的神经元变性。这项研究检验了以下假设：兴奋性毒性的初始和/或下游方面的中断应在与ELH相关的听力损失中提供听力保护。研究设计：这项研究测试了谷氨酸释放抑制剂利鲁唑和谷氨酸受体水平具有良好特性的抗炎和抗氧化溶剂二甲亚砜（DMSO）是否可以预防小鼠模型早期听力下降ELH。方法：Phex（Hyp-Duk）小鼠自发发展为ELH和产后听力下降。从出生后第6天（P6）开始，每天注射利鲁唑+ DMSO或仅注射DMSO。未经处理的突变体用作对照。在P21，P25和P30，通过记录听觉脑干反应来评估听力功能。制定了耳蜗功能指数以评估每个时间点的整体耳蜗功能。结果：与未治疗相比，DMSO提供了明显的听力保护（P <.05）。利鲁唑+ DMSO也显示出保护作用，但与单独使用DMSO在统计学上没有区别。没有观察到与利鲁唑的协同增效作用。结论：本研究证明了ELH动物模型的药理听力保护作用。结果支持这样的观点，即炎性（活性氧）损伤是兴奋性毒性途径的一部分，有助于ELH相关性听力损失的发展。

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