Apigenin alleviates neomycin-induced oxidative damage via the Nrf2 signaling pathway in cochlear hair cells

被引:7
|
作者
Jia, Gaogan
Mao, Huanyu
Zhang, Yanping
Ni, Yusu [1 ]
Chen, Yan [1 ]
机构
[1] Fudan Univ, Eye & ENT Hosp, ENT Inst, Shanghai 200031, Peoples R China
基金
国家重点研发计划; 中国国家自然科学基金;
关键词
apigenin; aminoglycosides; ototoxicity; oxidative stress; Nrf2 signaling pathway; CISPLATIN-INDUCED OTOTOXICITY; ROS; MITOCHONDRIA; ACTIVATION;
D O I
10.1007/s11684-021-0864-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:637 / 650
页数:14
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