ArticlePloS one2015
NaHS Protects Cochlear Hair Cells from Gentamicin-Induced Ototoxicity by Inhibiting the Mitochondrial Apoptosis Pathway.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Human induced pluripotent stem cell-derived inner ear organoids reveal hair cell damage and plasticity after cisplatin and gentamicin exposure.Disease models & mechanisms · 2026Article
- Involvement of cystathionine β-synthase in ATP-induced hydrogen sulfide production in cochlear outer hair cells.Journal of otology · 2026Article
- Vitamin D and sudden sensorineural hearing loss: emerging associations, mechanistic insights, and prospects for precision medicine - a review.Frontiers in nutrition · 2026Review
- An In Vitro Oxidative Stress Model of the Human Inner Ear Using Human-Induced Pluripotent Stem Cell-Derived Otic Progenitor Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Songorine ameliorates LPS-induced sepsis cardiomyopathy by Wnt/β-catenin signaling pathway-mediated mitochondrial biosynthesis.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Identification of Target Proteins Involved in Cochlear Hair Cell Progenitor Cytotoxicity following Gentamicin Exposure.Journal of clinical medicine · 2022Article
- In vivo real-time imaging reveals megalin as the aminoglycoside gentamicin transporter into cochlea whose inhibition is otoprotective.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Identification of a series of hair-cell MET channel blockers that protect against aminoglycoside-induced ototoxicity.JCI insight · 2021Article
- Icariin Treatment Protects Against Gentamicin-Induced Ototoxicity via Activation of the AMPK-SIRT3 Pathway.Frontiers in pharmacology · 2021Article
- Dihydromyricetin Protects Against Gentamicin-Induced Ototoxicity via PGC-1α/SIRT3 SignalingFrontiers in cell and developmental biology · 2020Article
- Enhanced mitochondrial membrane potential and ATP synthesis by photobiomodulation increases viability of the auditory cell line after gentamicin-induced intrinsic apoptosis.Scientific reports · 2019Article
- Novel compounds protect auditory hair cells against gentamycin-induced apoptosis by maintaining the expression level of H3K4me2.Drug delivery · 2018Article
- FoxO3a plays a key role in the protective effects of pomegranate peel extract against amikacin-induced ototoxicity.International journal of molecular medicine · 2017Article
- Bactericidal antibiotics promote oxidative damage and programmed cell death in sinonasal epithelial cells.International forum of allergy & rhinology · 2017Article
- NaHS Protects against the Impairments Induced by Oxygen-Glucose Deprivation in Different Ages of Primary Hippocampal Neurons.Frontiers in cellular neuroscience · 2017Article
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Authors and funding
4 authors.
Funding
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Abstract
Aminoglycoside antibiotics such as gentamicin could cause ototoxicity in mammalians, by inducing oxidative stress and apoptosis in sensory hair cells of the cochlea. Sodium hydrosulfide (NaHS) is reported to alleviate oxidative stress and apoptosis, but its role in protecting aminoglycoside-induced hearing loss is unclear. In this study, we investigated the anti-oxidant and anti-apoptosis effect of NaHS in in vitro cultured House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and isolated mouse cochlea. Results from cultured HEI-OC1 cells and cochlea consistently indicated that NaHS exhibited protective effects from gentamicin-induced ototoxicity, evident by maintained cell viability, hair cell number and cochlear morphology, reduced reactive oxygen species production and mitochondrial depolarization, as well as apoptosis activation of the intrinsic pathway. Moreover, in the isolated cochlear culture, NaHS was also demonstrated to protect the explant from gentamicin-induced mechanotransduction loss. Our study using multiple in vitro models revealed for the first time, the potential of NaHS as a therapeutic agent in protecting against aminoglycoside-induced hearing loss.
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