ArticleFrontiers of medicine2022
Apigenin alleviates neomycin-induced oxidative damage via the Nrf2 signaling pathway in cochlear hair cells.
Article in Frontiers of medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Temporal trends in cross-country inequalities of chronic kidney disease attributable to temperature exposure from 1990 to 2021.International urology and nephrology · 2025Article
- Versatile functions of methyl-CpG-binding domain 2 (MBD2) in cellular characteristics and differentiation.Molecular biology reports · 2025Review
- Mechanisms and otoprotective strategies of programmed cell death on aminoglycoside-induced ototoxicity.Frontiers in cell and developmental biology · 2023Review
- MicroRNA-141-3p attenuates oxidative stress-induced hepatic ischemia reperfusion injury via Keap1/Nrf2 pathway.Molecular biology reports · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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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.
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