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    Comparison of the protective efficacy between intratympanic dexamethasone and resveratrol treatments against cisplatin-induced ototoxicity: an experimental study
    (Springer, 2019) Simsek, Goekce; Tas, Burak Mustafa; Muluk, Nuray Bayar; Azman, Musa; Kilic, Rahmi
    Purpose The main aim of this study was to compare the efficacy of intratympanic administration of dexamethasone and resveratrol in preventing cisplatin ototoxicity by measuring acoustic brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). Methods Forty rats (80 ears) were divided into five groups. Cisplatin was administered intraperitoneally to the first group (n = 8). Group 2 (n = 8) received cisplatin after resveratrol had been administered intratympanically. Group 3 (n = 8) received cisplatin after dexamethasone had been administered intratympanically. Group 4 (n = 8) received cisplatin after sodium chloride (NaCl) had been given intratympanically. Group 5 (n = 8) received cisplatin after dimethylsulfoxide (DMSO) had been given intratympanically. ABR and DPOAE tests were performed on all groups before and 72 h after the procedure. Results ABR threshold values in rats that received dexamethasone and resveratrol were found to be less affected than those observed in the other post-cisplatin groups. ABR-IV and ABR-I-IV interval values were significantly reduced in rats that had been given dexamethasone and resveratrol compared to the other groups. After cisplatin treatment, otoacoustic emission (OAE) amplitudes were significantly decreased in Groups 1, 4, and 5 for all frequencies, while OAE values were sustained in the resveratrol and dexamethasone groups (Groups 2 and 3). At OAE frequency 5652, dexamethasone was more significantly associated with protective than resveratrol was, while no significant difference was found between the two groups at other OAE frequencies. Conclusion In conclusion, intratympanic dexamethasone and intratympanic resveratrol treatments may provide a significant protection against cisplatin-induced ototoxicity.

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