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Updated: Oct 9, 2025
Trans-Tympanic Drug Delivery for the Treatment of Ototoxicity
Published on: March 16, 2018
Apigenin alleviates neomycin-induced oxidative damage via the Nrf2 signaling pathway in cochlear hair cells
Gaogan Jia1,2, Huanyu Mao1,2, Yanping Zhang1,2
1ENT Institute and Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Abstract:
Oxidative stress plays an important role in the pathogenesis of aminoglycoside-induced hearing loss and represents a promising target for treatment. We tested the potential effect of apigenin, a natural flavonoid with anticancer, anti-inflammatory, and antioxidant activities, on neomycin-induced ototoxicity in cochlear hair cells in vitro. Results showed that apigenin significantly ameliorated the loss of hair cells and the accumulation of reactive oxygen species upon neomycin injury. Further evidence suggested that the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway was activated by apigenin treatment. Disruption of the Nrf2 axis abolished the effects of apigenin on the alleviation of oxidative stress and subsequent apoptosis of hair cells. This study provided evidence of the protective effect of apigenin on cochlear hair cells and its underlying mechanism.
Insights
Apigenin protects cochlear hair cells from neomycin-induced hearing loss by reducing oxidative stress. This natural flavonoid activates the Nrf2 pathway, offering a potential therapeutic strategy for ototoxicity.
Area of Science:
- Ototoxicity research
- Neuroscience
- Pharmacology
Background:
- Aminoglycoside ototoxicity is linked to oxidative stress.
- Cochlear hair cell damage is a primary cause of hearing loss.
- Natural compounds are explored for therapeutic potential.
Purpose of the Study:
- To investigate the protective effects of apigenin against neomycin-induced ototoxicity in cochlear hair cells.
- To elucidate the underlying mechanism involving the Nrf2 signaling pathway.
Main Methods:
- In vitro study using cochlear hair cells.
- Exposure to neomycin to induce ototoxicity.
- Treatment with apigenin and assessment of cell viability, reactive oxygen species (ROS) levels, and apoptosis.
- Analysis of the Nrf2 signaling pathway activation.
Main Results:
- Apigenin significantly reduced hair cell loss and ROS accumulation caused by neomycin.
- Apigenin treatment activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway.
- Disruption of the Nrf2 pathway negated apigenin's protective effects against oxidative stress and apoptosis.
Conclusions:
- Apigenin demonstrates a protective effect on cochlear hair cells against neomycin-induced ototoxicity.
- The protective mechanism involves the activation of the Nrf2 signaling pathway.
- Apigenin represents a potential therapeutic agent for preventing or treating aminoglycoside-induced hearing loss.
