氧化应激在老年性聋发病机制中的研究进展  

Progress of research of oxidative stress in the pathogenesis of presbycusis

作　　者：周颖东 张梦娴 王青玲 康浩然 郭向东[2] ZHOU Yingdong;ZHANG Mengxian;WANG Qingling;KANG Haoran;GUO Xiangdong(School of the 1st Clinical Medical Sciences,Henan University of Chinese Medicine,Zhengzhou 450046,Henan,China;Department of Otorhinolaryngology,The First Affiliated Hospital of Henan University of Chinese Medicine,Zhengzhou 450000,Henan,China)

机构地区：[1]河南中医药大学第一临床医学院,河南郑州450046 [2]河南中医药大学第一附属医院耳鼻咽喉科,河南郑州450000

出　　处：《山东大学耳鼻喉眼学报》2024年第1期72-78,91,共8页Journal of Otolaryngology and Ophthalmology of Shandong University

基　　金：国家自然科学基金项目(81403439);河南省科技攻关计划项目(222102310604);河南省中医药科学研究专项重点课题项目(20-21ZY1045);河南省高等学校重点科研项目(23A360028)。

摘　　要：老年性聋是由于内耳与听皮层老化导致的感音神经性听力损失。氧化应激在老年性聋的发生和发展中起着关键的作用。衰老过程中线粒体损伤与活性氧(reaetive oxygen species.ROS)的释放相互促进,导致氧化应激以及后续多种病理生理过程,如线粒体质量控制失衡、泛素-蛋白酶体系统障碍以及细胞程序性死亡等。抗氧化剂在清除ROS、调节线粒体功能和抑制细胞程序性死亡等方面发挥作用,对于老年性聋的防治展现出巨大潜能。总结近年来氧化应激及后续细胞过程在老年性聋中的发病机制以及抗氧化剂延缓老年性聋相关的研究进展,旨在为老年性聋的治疗提供理论基础。Presbycusis is a sensorineural hearing loss caused by senescence of the inner ear and auditory cortex.Oxidative stress plays a key role in the occurrence and development of presbycusis.During aging,mitochondrial damage and the release of reactive oxygen species(ROS)promote each other,leading to oxidative stress and a variety of subsequent pathophysiological processes such as an imbalance in mitochondrial quality control,ubiquitin-proteasome system disorders,and programmed cell death.Antioxidants play a role in scavenging ROS,regulating mitochondrial function and inhibiting programmed cell death,and have shown great potential in the prevention and treatment of presbycusis.This review focuses on the progress of research of oxidative stress and subsequent cellular processes in the pathogenesis of presbycusis and antioxidants in delaying presbycusis in order to provide a theoretical basis for its treatment.

关 键 词：老年性聋 氧化应激 线粒体质量控制 细胞程序性死亡 

分 类 号：R764.35[医药卫生—耳鼻咽喉科]