Department of Otolaryngology Head and Neck Surgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi, 710032, China.
BMC Neurosci. 2024 Jan 30;25(1):5. doi: 10.1186/s12868-024-00845-4.
The cochlear sympathetic system plays a key role in auditory function and susceptibility to noise-induced hearing loss (NIHL). The formation of reactive oxygen species (ROS) is a well-documented process in NIHL. In this study, we aimed at investigating the effects of a superior cervical ganglionectomy (SCGx) on NIHL in Sprague-Dawley rats.
We explored the effects of unilateral and bilateral Superior Cervical Ganglion (SCG) ablation in the eight-ten weeks old Sprague-Dawley rats of both sexes on NIHL. Auditory function was evaluated by auditory brainstem response (ABR) testing and Distortion product otoacoustic emissions (DPOAEs). Outer hair cells (OHCs) counts and the expression of α-adrenergic receptor (AR) in the rat cochlea using immunofluorescence analysis. Cells culture and treatment, CCK-8 assay, Flow cytometry staining and analysis, and western blotting were to explore the mechanisms of SCG fibers may have a protective role in NIHL.
We found that neither bilateral nor unilateral SCGx protected the cochlea against noise exposure. In HEI-OC1 cells, HO-induced oxidative damage and cell death were inhibited by the application of norepinephrine (NE). NE may prevent ROS-induced oxidative stress in OHCs and NIHL through the α-AR.
These results demonstrated that sympathetic innervation mildly affected cochlear susceptibility to acoustic trauma by reducing oxidative damage in OHCs through the α-AR. NE may be a potential therapeutic strategy for NIHL prevention.
耳蜗交感神经系统在听觉功能和对噪声性听力损失（NIHL）的易感性中起着关键作用。活性氧（ROS）的形成是 NIHL 中一个有据可查的过程。在这项研究中，我们旨在研究颈上交感神经节切除术（SCGx）对 Sprague-Dawley 大鼠 NIHL 的影响。
我们探索了单侧和双侧 Superior Cervical Ganglion（SCG）消融对 8-10 周龄雄性和雌性 Sprague-Dawley 大鼠 NIHL 的影响。通过听觉脑干反应（ABR）测试和畸变产物耳声发射（DPOAE）评估听觉功能。使用免疫荧光分析对大鼠耳蜗中的外毛细胞（OHC）计数和α-肾上腺素能受体（AR）的表达进行评估。细胞培养和处理、CCK-8 测定、流式细胞术染色和分析以及 Western blot 用于探索 SCG 纤维可能在 NIHL 中具有保护作用的机制。
我们发现双侧或单侧 SCGx 均不能保护耳蜗免受噪声暴露。在 HEI-OC1 细胞中，去甲肾上腺素（NE）的应用抑制了 HO 诱导的氧化损伤和细胞死亡。NE 可能通过α-AR 防止 OHC 中的 ROS 诱导的氧化应激和 NIHL。
这些结果表明，交感神经支配通过α-AR 减轻 OHC 中的氧化损伤，轻微影响耳蜗对声创伤的敏感性。NE 可能是预防 NIHL 的一种潜在治疗策略。
