ArticlePloS one2023
Dexamethasone treatment of murine auditory hair cells and cochlear explants attenuates tumor necrosis factor-α-initiated apoptotic damage.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Liposome-Encapsulated Rutin Attenuates Cisplatin-Induced Ototoxicity via Suppression of P53-Associated Oxidative Injury.Biomaterials research · 2026Article
- Audiometric changes following oral versus local gel foam steroid administration after stapedectomy in otosclerosis patients: a retrospective comparative study.Frontiers in medicine · 2026Article
- The role of serun lipid, cytokine production in sudden sensorineural hearing loss.Cytotechnology · 2025Article
- Intratympanic administration of dexamethasone attenuates radiation induced damage to middle ear mucosa.Scientific reports · 2025Article
- Porphyrin-based nanotechnology: a minimally invasive approach for drug delivery and cholesteatoma treatment.Frontiers in surgery · 2025Article
- The inflammatory and metabolic status of patients with sudden-onset sensorineural hearing loss.Frontiers in neurology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The most common cause of sensorineural hearing loss is damage of auditory hair cells. Tumor necrosis factor-alpha (TNF-α) is closely associated with sensorineural hearing loss. The present study examined the preconditioning effect of dexamethasone (DEX) on TNF-α-induced ototoxicity in mouse auditory hair cells (HEI-OC1) and cochlear explants. Treatment of HEI-OC1 with 10 ng/ml TNF-α for 24 h decreased cell viability, increased the accumulation of reactive oxygen species (ROS), and induced caspase-mediated apoptotic signaling pathways. Pretreatment with 10 nM DEX for 6 h before TNF-α exposure restored cell viability, decreased ROS accumulation, and attenuated apoptotic signaling activation induced by TNF-α. Incubation of cochlear explants with 20 ng/ml TNF-α for 24 h resulted in significant loss of both inner hair cells (IHCs) and outer hair cells (OHCs) and an increase in apoptotic activation accessed by annexin V staining. The cochlear explants pre-incubated with 10 nM DEX attenuated TNF-α ototoxicity in both IHCs and OHCs and apoptotic cell death. These results indicated that DEX plays a protective role in ototoxicity induced by TNF-α through attenuation of caspase-dependent apoptosis signaling pathway and ROS accumulation.
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