Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 mice

BackgroundSensorineural hearing loss (SNHL) is among the most common sensory disorders, significantly affecting various aspects of the quality of life of an individual. Oxidative stress and inflammation have been involved in the progression of various forms of SNHL and are potential pathological mec...

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Main Authors: Zhongwu Su, Yuyan Chen, Yu Liu, Jinyuan Cao, Jie Cui, Haitong Chen, Qi Li
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-03-01
Series:Frontiers in Neuroscience
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Online Access:https://www.frontiersin.org/articles/10.3389/fnins.2025.1563428/full
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author Zhongwu Su
Yuyan Chen
Yu Liu
Jinyuan Cao
Jie Cui
Haitong Chen
Qi Li
author_facet Zhongwu Su
Yuyan Chen
Yu Liu
Jinyuan Cao
Jie Cui
Haitong Chen
Qi Li
author_sort Zhongwu Su
collection DOAJ
description BackgroundSensorineural hearing loss (SNHL) is among the most common sensory disorders, significantly affecting various aspects of the quality of life of an individual. Oxidative stress and inflammation have been involved in the progression of various forms of SNHL and are potential pathological mechanisms of the disorder. However, the synergistic effects of oxidative stress and inflammation on cochlear function is not completely understood.MethodsWe explored the effects of oxidative stress and inflammation on cochlear damage and hearing impairment in male C57BL/6 mice aged 6 to 7 weeks. These in the experimental group were administered with oxidant Menadione bisulfite (MD) and the endotoxin lipopolysaccharide (LPS) via intraperitoneal route to induce oxidative stress and inflammation, whereas the control group received saline. The degree of cochlear damage was analyzed based on auditory thresholds, hair cells (HCs) loss, and the expression of protein markers related to oxidative stress, inflammation, necroptosis, and ferroptosis.ResultsAfter six days of alternating MD and LPS injections, there was a notable elevation in hearing thresholds, which was associated with a substantial loss of HCs and spiral ganglion cells. Immunofluorescence analysis demonstrated the activation of oxidative stress, inflammation, necroptosis, and ferroptosis signaling pathways after treatment. Notably, the administration of either MD or LPS alone did not result in significant changes.ConclusionThese findings indicate that the interaction between oxidative stress and inflammation may exacerbate cochlear damage and contribute to hearing loss, potentially through the activation of necroptosis and ferroptosis pathways. Our results may identify potential therapeutic targets for the management of SNHL.
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spelling doaj-art-a88572e1f2184b22a60cddad77281b8e2025-08-20T03:35:07ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2025-03-011910.3389/fnins.2025.15634281563428Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 miceZhongwu SuYuyan ChenYu LiuJinyuan CaoJie CuiHaitong ChenQi LiBackgroundSensorineural hearing loss (SNHL) is among the most common sensory disorders, significantly affecting various aspects of the quality of life of an individual. Oxidative stress and inflammation have been involved in the progression of various forms of SNHL and are potential pathological mechanisms of the disorder. However, the synergistic effects of oxidative stress and inflammation on cochlear function is not completely understood.MethodsWe explored the effects of oxidative stress and inflammation on cochlear damage and hearing impairment in male C57BL/6 mice aged 6 to 7 weeks. These in the experimental group were administered with oxidant Menadione bisulfite (MD) and the endotoxin lipopolysaccharide (LPS) via intraperitoneal route to induce oxidative stress and inflammation, whereas the control group received saline. The degree of cochlear damage was analyzed based on auditory thresholds, hair cells (HCs) loss, and the expression of protein markers related to oxidative stress, inflammation, necroptosis, and ferroptosis.ResultsAfter six days of alternating MD and LPS injections, there was a notable elevation in hearing thresholds, which was associated with a substantial loss of HCs and spiral ganglion cells. Immunofluorescence analysis demonstrated the activation of oxidative stress, inflammation, necroptosis, and ferroptosis signaling pathways after treatment. Notably, the administration of either MD or LPS alone did not result in significant changes.ConclusionThese findings indicate that the interaction between oxidative stress and inflammation may exacerbate cochlear damage and contribute to hearing loss, potentially through the activation of necroptosis and ferroptosis pathways. Our results may identify potential therapeutic targets for the management of SNHL.https://www.frontiersin.org/articles/10.3389/fnins.2025.1563428/fullsensorineural hearing lossoxidative stressinflammationcochleanecroptosisferroptosis
spellingShingle Zhongwu Su
Yuyan Chen
Yu Liu
Jinyuan Cao
Jie Cui
Haitong Chen
Qi Li
Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 mice
Frontiers in Neuroscience
sensorineural hearing loss
oxidative stress
inflammation
cochlea
necroptosis
ferroptosis
title Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 mice
title_full Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 mice
title_fullStr Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 mice
title_full_unstemmed Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 mice
title_short Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 mice
title_sort oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in c57bl 6 mice
topic sensorineural hearing loss
oxidative stress
inflammation
cochlea
necroptosis
ferroptosis
url https://www.frontiersin.org/articles/10.3389/fnins.2025.1563428/full
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