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Protective effect of (-)-epigallocatechin-3-gallate against cisplatin-induced ototoxicity

Published online by Cambridge University Press:  15 April 2014

S I Cho ,
J H Lee ,
J H Park  and
N Y Do
S I Cho*
Affiliation:
Department of Otolaryngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea
J H Lee
Affiliation:
Department of Otolaryngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea
J H Park
Affiliation:
Department of Otolaryngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea
N Y Do
Affiliation:
Department of Otolaryngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea
*
Address for correspondence: Dr S I Cho, Department of Otolaryngology-Head and Neck Surgery, Chosun University Hospital, 365 Pilmun-daero, Dong-gu, Gwangju 501-717, South Korea Fax: +82-62-225-2702 E-mail: [email protected]
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Abstract

Objective:

Ototoxicity due to cisplatin therapy interferes with treatment and often forces a reduction in the dosage, duration and frequency of the cisplatin therapy. (-)-Epigallocatechin-3-gallate is known to have the highest antioxidant potency among all tea catechins. This study aimed to investigate the effect of (-)-epigallocatechin-3-gallate on cisplatin ototoxicity in an auditory cell line: House Ear Institute-Organ of Corti 1 cells.

Methods:

Cultured House Ear Institute-Organ of Corti 1 cells were exposed to cisplatin with or without pre-treatment with (-)-epigallocatechin-3-gallate. Cell viability was evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Hoechst 33258 staining was used to identify cells undergoing apoptosis. Western blot analysis was conducted to determine whether (-)-epigallocatechin-3-gallate inhibited cisplatin-induced caspase activation. Intracellular reactive oxygen species production was examined to investigate whether (-)-epigallocatechin-3-gallate was capable of scavenging cisplatin-induced reactive oxygen species accumulation.

Results:

Cell viability significantly increased in cells pre-treated with (-)-epigallocatechin-3-gallate compared with cells exposed to cisplatin alone. Cisplatin increased cleaved caspase-3 on Western blot analysis; however, pre-treatment with (-)-epigallocatechin-3-gallate inhibited the expression of caspase-3. (-)-Epigallocatechin-3-gallate attenuated reactive oxygen species production and apoptosis in House Ear Institute-Organ of Corti 1 cells.

Conclusion:

(-)-Epigallocatechin-3-gallate protected against cisplatin cytotoxicity through anti-apoptotic and anti-oxidative effects. Therefore, (-)-epigallocatechin-3-gallate could play a preventive role in cisplatin-induced ototoxicity.

Keywords

Epigallocatechin-3-GallateCisplatinHearing LossApoptosisIn VitroCell Culture
Type
Main Articles
Information
The Journal of Laryngology & Otology , Volume 128 , Issue 4 , April 2014 , pp. 350 - 355
Copyright
Copyright © JLO (1984) Limited 2014 

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