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

Gi Jung Im, Jiwon Chang, Sehee Lee, June Choi, Hak Hyun Jung, Hyung Min Lee, Sung Hoon Ryu, Su Kyoung Park, Jin Hwan Kim, Hyung Jong Kim

Research output: Contribution to journalArticle

8 Citations (Scopus)

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 μM of edaravone prior to application of 15 μM 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>.

Original languageEnglish
Pages (from-to)113-118
Number of pages6
JournalHearing Research
Volume330
DOIs
Publication statusPublished - 2015 Dec 1

Keywords

  • Apoptosis
  • Cell culture
  • Cisplatin
  • Edaravone
  • Ototoxicity

ASJC Scopus subject areas

  • Sensory Systems

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