Department of Otolaryngology, Ajou University Faculty of Medicine, Suwon, Korea.
Department of Otolaryngology, Ajou University Faculty of Medicine, Suwon, Korea; Department of Biomedical Sciences, BK21 Plus Research Center for Biomedical Sciences, Ajou University Graduate Faculty of Medicine, Suwon, Korea; Department of Medical Sciences, Ajou University Graduate Faculty of Medicine, Suwon, Korea.
J Int Adv Otol. 2023 Jan;19(1):10-15. doi: 10.5152/iao.2023.21659.
Stress could be a contributing cause of sudden hearing loss. This study intended to develop an animal model of stress-induced sudden hearing loss and to evaluate the effects of dexamethasone.
Two stress models (I and II) for rats were designed using various stressors and modified by adjusting the stress protocol to increase the threshold significantly. For the stress model with a significant increase in threshold after stress exposure, changes in cortisol levels according to stress exposure were measured. The threshold shift and the change in the cellular structure associated with stress exposure and dexamethasone administration were analyzed.
While hearing thresholds increased only at 16 kHz in rats of stress model I (n=10), the thresholds increased at 16 and 32 kHz in rats of stress model II (n=16). Cortisol level increased after stress exposure (P = .015) in stress model II. Among stress model II rats (stress only and stress+dexamethasone groups), the threshold shift at 16 kHz significantly decreased 1 day after dexamethasone injection in the stress+dexamethasone group (n=8). Histologically, the cochlear cellularity of the stress+dexamethasone group was more compact than that of the stressonly group (n=8).
Our preliminary study presented the development of an animal model of stress-induced sudden hearing loss and the positive results of steroids in terms of hearing recovery.
压力可能是突发性听力损失的一个促成因素。本研究旨在建立应激诱导突发性听力损失的动物模型，并评估地塞米松的作用。
设计了两种大鼠应激模型（I 型和 II 型），使用不同的应激源，并通过调整应激方案来显著增加阈值进行了修改。对于应激后阈值显著增加的应激模型，测量了皮质醇水平随应激暴露的变化。分析了应激暴露和地塞米松给药后阈值变化和与应激相关的细胞结构变化。
应激模型 I（n=10）中，大鼠的听力阈值仅在 16 kHz 处升高，而应激模型 II（n=16）中大鼠的阈值在 16 和 32 kHz 处升高。皮质醇水平在应激暴露后升高（P =.015）应激模型 II。在应激模型 II 大鼠（仅应激组和应激+地塞米松组）中，应激+地塞米松组在注射地塞米松后 1 天，16 kHz 的阈值变化显著降低（n=8）。组织学上，应激+地塞米松组的耳蜗细胞结构比仅应激组更紧凑（n=8）。
我们的初步研究提出了应激诱导突发性听力损失的动物模型的建立以及类固醇在听力恢复方面的积极结果。
