title: NaHS Protects Cochlear Hair Cells from Gentamicin-Induced Ototoxicity by Inhibiting the Mitochondrial Apoptosis Pathway.
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.
authors: Department of Otology, Shengjing Hospital Affiliated to China Medical University, Shenyang 110004, Liaoning, China.
authors: Yaodong
authors: Y
authors: Dong
authors: Department of Otology, Shengjing Hospital Affiliated to China Medical University, Shenyang 110004, Liaoning, China.
authors: Dongliang
authors: D
authors: Liu
authors: Department of Otology, Shengjing Hospital Affiliated to China Medical University, Shenyang 110004, Liaoning, China.
authors: Yue
authors: Y
authors: Hu
authors: Department of Otology, Shengjing Hospital Affiliated to China Medical University, Shenyang 110004, Liaoning, China.
authors: Xiulan
authors: X
authors: Ma
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000633:toxicity*; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002452:Cell Count; D002470:Cell Survival / Q000187:drug effects; D005786:Gene Expression Regulation; D005839:Gentamicins / Q000037:antagonists & inhibitors / Q000633:toxicity*; D006198:Hair Cells, Auditory / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D040542:Mechanotransduction, Cellular / Q000187:drug effects; D051379:Mice; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D009924:Organ Culture Techniques; D018384:Oxidative Stress / Q000187:drug effects; D061251:Primary Cell Culture; D020011:Protective Agents / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D013440:Sulfides / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D000900:Anti-Bacterial Agents; D005839:Gentamicins; D020011:Protective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D013440:Sulfides; D051028:bcl-2-Associated X Protein; C052617:Bcl2 protein, mouse; C505409:Casp3 protein, mouse; D053148:Caspase 3; C025451:sodium bisulfide