title: Protective effect of (-)-epigallocatechin-3-gallate against cisplatin-induced ototoxicity.
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.
  
  
  CONCLUSIONS
  (-)-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.
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea.
authors.forename: S I
authors.initials: SI
authors.lastname: Cho
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea.
authors.forename: J H
authors.initials: JH
authors.lastname: Lee
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea.
authors.forename: J H
authors.initials: JH
authors.lastname: Park
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea.
authors.forename: N Y
authors.initials: NY
authors.lastname: Do
mesh_terms: D002945:Cisplatin / Q000633:toxicity / Q000009:adverse effects; D002392:Catechin / Q000031:analogs & derivatives / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D000081015:Ototoxicity / Q000517:prevention & control; D002470:Cell Survival / Q000187:drug effects; D000818:Animals; D009925:Organ of Corti / Q000187:drug effects / Q000473:pathology; D000970:Antineoplastic Agents / Q000009:adverse effects / Q000633:toxicity; D000975:Antioxidants / Q000494:pharmacology; D051379:Mice; D002460:Cell Line; D053148:Caspase 3 / Q000378:metabolism
chemical_list: D002945:Cisplatin; D002392:Catechin; C045651:epigallocatechin gallate; D017382:Reactive Oxygen Species; D000970:Antineoplastic Agents; D000975:Antioxidants; D053148:Caspase 3
keywords: Apoptosis; Cell Culture; Cisplatin; Epigallocatechin-3-Gallate; Hearing Loss; In Vitro