Protective effect of gallic acid against cisplatin-induced ototoxicity in rats.
Acoustic Stimulation
Animals
Cisplatin
/ toxicity
Cochlea
/ drug effects
Disease Models, Animal
Female
Gallic Acid
/ administration & dosage
Immunohistochemistry
Injections, Intraperitoneal
Otoacoustic Emissions, Spontaneous
/ drug effects
Protective Agents
/ administration & dosage
Rats
Rats, Sprague-Dawley
Cisplatin-induced ototoxicity
DPOAE
EOAPD
Estresse oxidativo
Gallic acid
Ototoxicidade induzida por cisplatina
Oxidative stress
Ácido gálico
Journal
Brazilian journal of otorhinolaryngology
ISSN: 1808-8686
Titre abrégé: Braz J Otorhinolaryngol
Pays: Brazil
ID NLM: 101207337
Informations de publication
Date de publication:
Historique:
received:
28
02
2018
accepted:
08
03
2018
pubmed:
21
4
2018
medline:
10
7
2019
entrez:
21
4
2018
Statut:
ppublish
Résumé
Cisplatin is an antineoplastic agent widely used in the treatment of a variety of cancers. Ototoxicity is one of the main side-effects restricting the use of cisplatin. The purpose of this study was to investigate the protective efficacy of gallic acid, in biochemical, functional and histopathological terms, against ototoxicity induced by cisplatin. Twenty-eight female Sprague Dawley rats were included. Rats were randomly assigned into four groups of seven animals each. Cisplatin group received a single intraperitoneal dose of 15mg/kg cisplatin. Gallic acid group received intraperitoneal gallic acid at 100mg/kg for five consecutive days. Cisplatin+gallic acid group received intraperitoneal gallic acid at 100mg/kg for five consecutive days and a single intraperitoneal dose of 15mg/kg cisplatin at 3rd day. A control group received 1mL intraperitoneal saline solution for five consecutive days. Prior to drug administration, all rats were exposed to the distortion product otoacoustic emissions test. The test was repeated on the 6th day of the study. All rats were then sacrificed; the cochleas were removed and set aside for biochemical and histopathological analyses. In cisplatin group, Day 6 signal noise ratio values were significantly lower than those of the other groups. Also, malondialdehyde levels in cochlear tissues were significantly higher, superoxide dismutase and glutathione peroxidase activities were significantly lower compared to the control group. Histopathologic evaluation revealed erosion in the stria vascularis, degeneration and edema in the connective tissue layer in endothelial cells, impairment of outer hair cells and a decrease in the number of these calls. In the cisplatin+gallic acid group, this biochemical, histopathological and functional changes were reversed. In the light of our findings, we think that gallic acid may have played a protective role against cisplatin-induced ototoxicity in rats, as indicated by the distortion product otoacoustic emissions test results, biochemical findings and immunohistochemical analyses.
Identifiants
pubmed: 29673779
pii: S1808-8694(18)30088-0
doi: 10.1016/j.bjorl.2018.03.001
pmc: PMC9442874
pii:
doi:
Substances chimiques
Protective Agents
0
Gallic Acid
632XD903SP
Cisplatin
Q20Q21Q62J
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
267-274Informations de copyright
Copyright © 2018 Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial. Published by Elsevier Editora Ltda. All rights reserved.
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