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Redox Biol. 2020 Jan;29:101406. doi: 10.1016/j.redox.2019.101406. Epub 2019 Dec 14.
2
Auditory metabolomics, an approach to identify acute molecular effects of noise trauma.听觉代谢组学，一种识别噪声创伤急性分子效应的方法。
Sci Rep. 2019 Jun 25;9(1):9273. doi: 10.1038/s41598-019-45385-8.
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Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS.糖酵解上调作为 ALS 的一种代偿机制具有神经保护作用。
Elife. 2019 Jun 10;8:e45114. doi: 10.7554/eLife.45114.
4
The TLR-4/NF-κB signaling pathway activation in cochlear inflammation of rats with noise-induced hearing loss.噪声性听力损失大鼠耳蜗炎症中TLR-4/NF-κB信号通路的激活
Hear Res. 2019 Aug;379:59-68. doi: 10.1016/j.heares.2019.04.012. Epub 2019 May 3.
5
Modulation of miR-34a/SIRT1 signaling protects cochlear hair cells against oxidative stress and delays age-related hearing loss through coordinated regulation of mitophagy and mitochondrial biogenesis.miR-34a/SIRT1 信号的调节通过协调调控细胞自噬和线粒体生物发生来保护耳蜗毛细胞免受氧化应激，并延缓年龄相关性听力损失。
Neurobiol Aging. 2019 Jul;79:30-42. doi: 10.1016/j.neurobiolaging.2019.03.013. Epub 2019 Mar 27.
6
The histone methyltransferase G9a regulates tolerance to oxidative stress-induced energy consumption.组蛋白甲基转移酶 G9a 调节氧化应激诱导的能量消耗的耐受性。
PLoS Biol. 2019 Mar 12;17(3):e2006146. doi: 10.1371/journal.pbio.2006146. eCollection 2019 Mar.
7
Targeting dysregulation of redox homeostasis in noise-induced hearing loss: Oxidative stress and ROS signaling.靶向调控噪声性听力损失中的氧化还原平衡失调：氧化应激和 ROS 信号转导。
Free Radic Biol Med. 2019 May 1;135:46-59. doi: 10.1016/j.freeradbiomed.2019.02.022. Epub 2019 Feb 22.
8
Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease.氧化应激、葡萄糖代谢功能障碍与阿尔茨海默病。
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9
Inhibition of Histone Methyltransferase G9a Attenuates Noise-Induced Cochlear Synaptopathy and Hearing Loss.组蛋白甲基转移酶 G9a 的抑制可减轻噪声诱导的耳蜗突触病和听力损失。
J Assoc Res Otolaryngol. 2019 Jun;20(3):217-232. doi: 10.1007/s10162-019-00714-6. Epub 2019 Feb 1.
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Mol Neurobiol. 2019 Aug;56(8):5950-5969. doi: 10.1007/s12035-019-1493-6. Epub 2019 Jan 28.

葡萄糖可保护耳蜗毛细胞免受氧化应激，减轻小鼠噪声性听力损失。

Glucose Protects Cochlear Hair Cells Against Oxidative Stress and Attenuates Noise-Induced Hearing Loss in Mice.

机构信息

Department of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510120, China.

Institute of Hearing and Speech-Language Science, Sun Yat-sen University, Guangzhou, 510120, China.

出版信息

Neurosci Bull. 2021 May;37(5):657-668. doi: 10.1007/s12264-020-00624-1. Epub 2021 Jan 7.

DOI:10.1007/s12264-020-00624-1
PMID:33415566
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8099978/
Abstract

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 HO-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.

摘要

氧化应激是噪声性听力损失（NIHL）发病机制的关键决定因素。鉴于细胞抵御氧化应激是一个耗能过程，本研究旨在探讨通过葡萄糖补充增加能量供应是否能保护耳蜗毛细胞免受氧化应激并减轻 NIHL。我们的结果表明，葡萄糖补充减少了噪声诱导的活性氧（ROS）的形成，从而减轻了 CBA/J 小鼠的噪声诱导的外毛细胞、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，同时减轻了 HO 诱导的 ROS 产生和细胞毒性。此外，葡萄糖转运蛋白 1 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。这些发现表明，能量供应对于氧化应激抵抗至关重要，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。