Oxidative stress is the key determinant in the pathogenesis of noise-induced hearing loss (NIHL). Given that cellular defense against oxidative stress is an energy-consuming process, the aim of the present study was to investigate whether increasing energy availability by glucose supplementation protects cochlear hair cells against oxidative stress and attenuates NIHL. Our results revealed that glucose supplementation reduced the noise-induced formation of reactive oxygen species (ROS) and consequently attenuated noise-induced loss of outer hair cells, inner hair cell synaptic ribbons, and NIHL in CBA/J mice. In cochlear explants, glucose supplementation increased the levels of ATP and NADPH, as well as attenuating H₂O₂-induced ROS production and cytotoxicity. Moreover, pharmacological inhibition of glucose transporter type 1 activity abolished the protective effects of glucose against oxidative stress in HEI-OC1 cells. These findings suggest that energy availability is crucial for oxidative stress resistance and glucose supplementation offers a simple and effective approach for the protection of cochlear hair cells against oxidative stress and NIHL.

氧化应激是噪声性听力损失 (NIHL) 发病机制的关键决定因素。鉴于细胞对氧化应激的防御是一个消耗能量的过程，本研究的目的是研究通过补充葡萄糖来增加能量可用性是否可以保护耳蜗毛细胞免受氧化应激并减轻 NIHL。我们的研究结果表明，葡萄糖补充剂减少了噪音引起的活性氧 (ROS) 的形成，从而减弱了 CBA/J 小鼠中由噪音引起的外毛细胞、内毛细胞突触带和 NIHL 的损失。在耳蜗外植体中，葡萄糖补充增加了 ATP 和 NADPH 的水平，并减弱了 H ₂ O ₂- 诱导的 ROS 产生和细胞毒性。此外，葡萄糖转运蛋白 1 型活性的药理学抑制消除了葡萄糖对 HEI-OC1 细胞氧化应激的保护作用。这些研究结果表明，能量可用性对于抗氧化应激至关重要，而葡萄糖补充为保护耳蜗毛细胞免受氧化应激和 NIHL 提供了一种简单有效的方法。