Objective: Caffeic acid phenethyl ester (CAPE) is known to reduce the generation of oxygen-derived free radicals, which is a major mechanism of aminoglycoside-induced ototoxicity. The objective of the present study was to evaluate the effects of CAPE on neomycin-induced ototoxicity in zebrafish (Brn3c: EGFP). Methods: Five-day post-fertilization zebrafish larvae (n= 10) were exposed to 125. μM neomycin and one of the following CAPE concentrations for 1. h: 50, 100, 250, 500, or 1000. μM. Ultrastructural changes were evaluated using scanning electron microscopy (SEM). The terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL) assay and 2-[4-(dimethylamino)styryl]- N-ethylpyridiniumiodide (DASPEI) assay were performed for evaluation of apoptosis and mitochondrial damage. Results: CAPE decreased neomycin-induced hair cell loss in the neuromasts (500. μM CAPE: 12.7 ± 1.1 cells, 125. μM neomycin only: 6.3 ± 1.1 cells; n= 10, P < 0.05). In the ultrastructural analysis, structures of mitochondria and hair cells were preserved when exposed to 125. μM neomycin and 500. μM CAPE. CAPE decreased apoptosis and mitochondrial damage. Conclusion: In the present study, CAPE attenuated neomycin-induced hair cell damage in zebrafish. The results of the current study suggest that neomycin induces apoptosis, and the apoptotic cell death can be prevented by treatment with CAPE in zebrafish.
|Number of pages||5|
|Journal||International Journal of Pediatric Otorhinolaryngology|
|Publication status||Published - 2014 Jan 1|
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health