Zheng Zeyu, Zhang Peng, Fu Yang, Jiang Yihong, Zhu Jing, Wang Fei, Li Shaoheng, Zhang Zhuoru, Chang Tong, Li Tian, Zhang Min, Ruan Bai, Wang Xiaocheng
Center of Clinical Aerospace Medicine, School of Aerospace Medicine, Key Laboratory of Aerospace Medicine of Ministry of Education, Air Force Medical University, Xi'an, Shaanxi, China.
Department of Aviation Medicine, Xijing Hospital, Xi'an, China.
Cell Biol Int. 2025 Mar;49(3):262-276. doi: 10.1002/cbin.12264. Epub 2024 Dec 1.
Hidden hearing loss (HHL) is characterized by normal audiometric thresholds but impaired auditory function, particularly in noisy environments. In vivo, we employed auditory brainstem response (ABR) testing and ribbon synapses counting to assess changes in mouse hearing function, and observed the morphology of hair cells through scanning electron microscopy. SRT1720 was administered to the cochlea via round window injection. In vitro, western blot analysis and RT-qPCR were used, and Lenti-shNrf2 was used to knockdown Nrf2 expression. In addition, various oxidative stress indicators were detected by immunofluorescence, kit-based assays, and flow cytometry. ABR measurement of HHL mouse showed a significant increase in hearing threshold, as well as a decrease and delay in the I wave amplitude and latency on the first day after noise exposure. Histological observation showed a significant loss of ribbon synapses and stereocilia lodging. HHL mice exhibited oxidative stress, which was reduced by pretreatment with SRT1720. Additionally, SRT1720 could reduce hydrogen peroxide-induced oxidative stress in HEI-OC1 cells through activating the SIRT1/Nrf2 pathway. Subsequent experiments with Nrf2 knockdown confirmed the importance of this pathway. findings highlight oxidative stress as the primary contributor to HHL, with the SIRT1/Nrf2 signaling pathway emerging as a promising therapeutic target for alleviating HHL.
隐匿性听力损失(HHL)的特征是听阈正常但听觉功能受损,尤其是在嘈杂环境中。在体内,我们采用听性脑干反应(ABR)测试和带状突触计数来评估小鼠听力功能的变化,并通过扫描电子显微镜观察毛细胞的形态。通过圆窗注射将SRT1720注入耳蜗。在体外,使用蛋白质免疫印迹分析和逆转录定量聚合酶链反应(RT-qPCR),并使用慢病毒短发夹RNA(Lenti-shNrf2)敲低Nrf2表达。此外,通过免疫荧光、试剂盒检测和流式细胞术检测各种氧化应激指标。对HHL小鼠的ABR测量显示,噪声暴露后第一天听力阈值显著升高,I波振幅降低且潜伏期延长。组织学观察显示带状突触显著丢失和静纤毛倒伏。HHL小鼠表现出氧化应激,而SRT1720预处理可减轻这种氧化应激。此外,SRT1720可通过激活SIRT1/Nrf2途径减轻过氧化氢诱导的HEI-OC1细胞氧化应激。随后的Nrf2敲低实验证实了该途径的重要性。这些发现突出了氧化应激是HHL的主要促成因素,而SIRT1/Nrf2信号通路有望成为缓解HHL的治疗靶点。