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Protective role of edaravone against cisplatin-induced ototoxicity in an auditory cell line

Authors
Im, Gi JungChang, JiwonLee, SeheeChoi, JuneJung, Hak HyunLee, Hyung MinRyu, Sung HoonPark, Su KyoungKim, Jin HwanKim, Hyung-Jong
Issue Date
12월-2015
Publisher
ELSEVIER
Keywords
Edaravone; Cisplatin; Ototoxicity; Cell culture; Apoptosis
Citation
HEARING RESEARCH, v.330, pp.113 - 118
Indexed
SCIE
SCOPUS
Journal Title
HEARING RESEARCH
Volume
330
Start Page
113
End Page
118
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/91818
DOI
10.1016/j.heares.2015.08.004
ISSN
0378-5955
Abstract
Edaravone is a neuroprotective agent with a potent free radical scavenging and antioxidant actions. In the present study we investigated the influence of edaravone on cisplatin ototoxicity in auditory cells. Cell viability was determined using a 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide cell proliferation assay. Oxidative stress and apoptosis were assessed by reactive oxygen species (ROS) measurement, Hoechst 33258 staining, caspase-3 activity assay, and immunoblotting of PARP. Pretreatment with 100 mu M of edaravone prior to application of 15 mu M of cisplatin increased cell viability after 48 h of incubation in HEI-OC1 cells (from 51.9% to 64. 6% viability) and also, attenuated the cisplatin-induced increase in reactive oxygen species (ROS) (from 2.3 fold to 1.9 fold). Edaravone also decreased the activation of caspase-3 and reduced levels of cleaved poly-ADP-ribose polymerase (PARP). We propose that edaravone protects against cisplatin-induced ototoxicity by preventing apoptosis, and limiting ROS production in HEI-OC1 cells. This article is part of a Special Issue entitled <IEB Kyoto>. (C) 2015 Elsevier B.V. All rights reserved.
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