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通过调节SIRT1表达,AIMP1在老年性听力损失的小鼠中发挥着听力保护作用

Haisen Peng¹, Jiali Liu¹, Yuehui Liu¹

¹Department of Otolaryngology, Head and Neck Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, No.1, Minde Road, Donghu district, Nanchang, Jiangxi, 330006, China.

|August 21, 2025

概括

AIMP1过度表达通过促进耳毛细胞的线粒细胞衰减和抑制耳毛细胞衰减来防止与年龄相关的听力损失. 这表明AIMP1是ARHL的一个有前途的治疗点.

科学领域:

眼科学
分子生物学
细胞生物学

背景情况:

与年龄相关的听力损失 (ARHL) 是一种复杂的感觉神经疾病,其病因不明.
研究新的分子点对于开发有效的ARHL治疗至关重要.

研究的目的:

阐明AIMP1在ARHL的发病过程中的特定作用.
确定AIMP1是否可以作为ARHL的治疗点.

主要方法:

HEI-OC1细胞受到过氧化 (H2O2) 诱导的氧化应激.
评估了细胞活力,细胞亡,活性氧物种 (ROS),甲酸 (MDA) 和铜含量.
通过Western涂抹和免疫光分析了与线粒细胞衰变和cuproptosis有关的蛋白质表达.
在实体ARHL小鼠模型中使用了D- 银糖.

主要成果:

在受H2O2治疗的细胞中,AIMP1过度表达增强了细胞活力,降低了氧化应激 (ROS,MDA),降低了细胞亡和铜水平.
参与线粒细胞衰变 (PINK1,帕金) 和亡 (FDX1,DLAT,DLST) 的AIMP1调节蛋白.
在ARHL小鼠中,AIMP1过度表达改善了耳损伤和部分恢复听力.

结论:

通过AIMP1上调SIRT1,促进PINK1/帕金基介导的线粒并抑制耳毛细胞的缩.
AIMP1显示出对ARHL的保护作用,强调其作为治疗点的潜力.

关键词:

一个 AIMP1 年龄相关的听力损失菌病甲状腺氧化应激一个SIRT1

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