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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: chosi@chosun.ac.kr
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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

Information

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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References

1Hartmann, JT, Lipp, HP. Toxicity of platinum compounds. Expert Opin Pharmacother 2003;4:889–901CrossRefGoogle ScholarPubMed
2Hamers, FP, Klis, SF, Gispen, WH, Smoorenburg, GF. Application of a neuroprotective ACTH(4–9) analog to affect cisplatin ototoxicity: an electrocochleographic study in guinea pigs. Eur Arch Otorhinolaryngol 1994;251:23–9Google Scholar
3Dehne, N, Lautemann, J, Petrat, F, Rauen, U, de Groot, H. Cisplatin ototoxicity: involvement of iron and enhanced formation of superoxide anion radicals. Toxicol Appl Pharmacol 2001;174:27–34CrossRefGoogle ScholarPubMed
4Pigeolet, E, Corbisier, P, Houbion, A, Lambert, D, Michiels, C, Raes, M et al. Glutathione peroxidase, superoxide dismutase, and catalase inactivation by peroxides and oxygen derived free radicals. Mech Ageing Dev 1990;51:283–97CrossRefGoogle ScholarPubMed
5Clerici, WJ, DiMartino, DL, Prasad, MR. Direct effects of reactive oxygen species on cochlear outer hair cell shape in vitro. Hear Res 1995;84:30–40Google Scholar
6Rybak, LP, Kelly, T. Ototoxicity: bioprotective mechanisms. Curr Opin Otolaryngol Head Neck Surg 2003;11:328–33Google Scholar
7Wei, H, Meng, Z. Protective effects of epigallocatechin-3-gallate against lead-induced oxidative damage. Hum Exp Toxicol 2011;30:1521–8CrossRefGoogle ScholarPubMed
8Guo, Q, Zhao, B, Li, M, Shen, S, Xin, W. Studies on protective mechanisms of four components of green tea polyphenols against lipid peroxidation in synaptosomes. Biochim Biophys Acta 1996;1304:210–22CrossRefGoogle ScholarPubMed
9Mandel, SA, Amit, T, Kalfon, L, Reznichenko, L, Youdim, MB. Targeting multiple neurodegenerative diseases etiologies with multimodel-acting green tea catechins. J Nutr 2008;133:1578–83SGoogle Scholar
10Landis-Piwowar, KR, Huo, C, Chen, D, Milacic, V, Shi, G, Chan, TH et al. A novel prodrug of the green tea polyphenol (-)-epigallocatechin-3-gallate as a potential anticancer agent. Cancer Res 2007;67:4303–10CrossRefGoogle ScholarPubMed
11Choi, YT, Jung, CH, Lee, SR, Bae, JH, Baek, WK, Suh, MH et al. The green tea (-)-epigallocatechin gallate attenuates beta-amyloid-induced neurotoxicity in cultured hippocampal neurons. Life Sci 2001;70:603–14Google Scholar
12Nie, G, Cao, Y, Zhao, B. Protective effects of green tea polyphenols and their major component, (-)-epigallocatechin-3-gallate (EGCG), on 6-hydroxydopamine-induced apoptosis in PC12 cells. Redox Rep 2002;7:171–7Google Scholar
13Sheng, R, Gu, ZL, Xie, ML, Zhou, WX, Guo, CY. Epigallocatechin gallate protects H9c2 cardiomyoblasts against hydrogen dioxides-induced apoptosis and telomere attrition. Eur J Pharmacol 2010;641:199–206CrossRefGoogle ScholarPubMed
14Yao, K, Ye, P, Zhang, L, Tan, J, Tang, X, Zhang, Y. Epigallocatechin gallate protects against oxidative stress-induced mitochondria-dependent apoptosis in human lens epithelial cells. Mol Vis 2008;14:217–23Google Scholar
15Park, SJ, Park, SH, Chang, JW, Choi, J, Jung, HH, Im, GJ. Protective effect of klotho protein against cisplatin ototoxicity in an auditory cell line. J Laryngol Otol 2012;126:1003–9CrossRefGoogle Scholar
16Chen, FQ, Hill, K, Guan, YJ, Schacht, J, Sha, SH. Activation of apoptotic pathways in the absence of cell death in an inner-ear immortomouse cell line. Hear Res 2012;284:33–41CrossRefGoogle Scholar
17Wang, D, Lippard, SJ. Cellular processing of platinum anticancer drugs. Nat Rev Drug Discov 2005;4:307–20CrossRefGoogle ScholarPubMed
18Lee, JE, Nakagawa, T, Kim, TS, Endo, T, Shiga, A, Iguchi, F et al. Role of reactive radicals in degeneration of the auditory system of mice following cisplatin treatment. Acta Otolaryngol 2004;124:1131–5Google Scholar
19Alam, SA, Ikeda, K, Oshima, T, Suzuki, M, Kawase, T, Kikuchi, T et al. Cisplatin-induced apoptotic cell death in Mongolian gerbil cochlea. Hear Res 2000;141:28–38Google Scholar
20Watanabe, K, Inai, S, Jinnouchi, K, Baba, S, Yagi, T. Expression of caspase-activated deoxyribonuclease (CAD) and caspase 3 (CPP32) in the cochlea of cisplatin (CDDP)-treated guinea pigs. Auris Nasus Larynx 2003;30:219–25CrossRefGoogle ScholarPubMed
21Wang, J, Ladrech, S, Pujol, R, Brabet, P, Van De Water, TR, Puel, JL. Caspase inhibitors, but not c-Jun NH 2-terminal kinase inhibitor treatment, prevent cisplatin-induced hearing loss. Cancer Res 2004;64:9217–24Google Scholar
22Rybak, LP, Whitworth, CA. Ototoxicity: therapeutic opportunities. Drug Discov Today 2005;10:1313–21Google Scholar
23Rybak, LP, Whitworth, CA, Mukherjea, D, Ramkumar, V. Mechanisms of cisplatin-induced ototoxicity and prevention. Hear Res 2007;226:157–67Google Scholar
24Ahmad, N, Feyes, DK, Nieminen, AL, Agarwal, R, Mukhtar, H. Green tea constituent epigallocatechin-3-gallate and induction of apoptosis and cell cycle arrest in human carcinoma cells. J Natl Cancer Inst 1997;89:1881–6CrossRefGoogle ScholarPubMed
25Lin, YL, Lin, JK. (-)-Epigallocatechin-3-gallate blocks the induction of nitric oxide synthase by down-regulating lipopolysaccharide-induced activity of transcription factor nuclear factor-kappaB. Mol Pharmacol 1997;52:465–72Google Scholar
26Mukhtar, H, Ahmad, N. Tea polyphenols: prevention of cancer and optimizing health. Am J Clin Nutr 2000;71:1698–702SCrossRefGoogle ScholarPubMed
27Kim, CH, Kang, SU, Pyun, J, Lee, MH, Hwang, HS, Lee, H. Epicatechin protects auditory cells against cisplatin-induced death. Apoptosis 2008;13:1184–94Google Scholar
28Chen, D, Milacic, V, Chen, MS, Wan, SB, Lam, WH, Huo, C et al. Tea polyphenols, their biological effects and potential molecular targets. Histol Histopathol 2008;23:487–96Google Scholar
29Koh, SH, Kwon, H, Kim, KS, Kim, J, Kim, MH, Yu, HJ et al. Epigallocatechin gallate prevents oxidative-stress-induced death of mutant Cu/Zn-superoxide dismutase (G93A) motoneuron cells by alteration of cell survival and death signals. Toxicology 2004;202:213–25Google Scholar
30Jin, CF, Shen, SR Sr, Zhao, BL. Different effects of five catechins on 6-hydroxydopamine-induced apoptosis in PC12 cells. J Agric Food Chem 2001;49:6033–8Google Scholar
31Choi, JH, Rhee, IK, Park, KY, Park, KY, Kim, JK, Rhee, SJ. Action of green tea catechin on bone metabolic disorder in chronic cadmium-poisoned rats. Life Sci 2003;73:1479–89Google Scholar
32Young, IS, Woodside, JV. Antioxidants in health and disease. J Clin Pathol 2001;54:176–86Google Scholar
33Nie, G, Jin, C, Cao, Y, Shen, S, Zhao, B. Distinct effects of tea catechins on 6-hydroxydopamine-induced apoptosis in PC12 cells. Arch Biochem Biophys 2002;397:84–90Google Scholar
34Gonçalves, MS, Silveira, AF, Teixeira, AR, Hyppolito, MA. Mechanisms of cisplatin ototoxicity: theoretical review. J Laryngol Otol 2013;127:536–41Google Scholar