PUBLICATION

Protective effects of caffeic acid phenethyl ester (CAPE) against neomycin-induced hair cell damage in zebrafish

Authors
Park, M.K., Im, G.J., Chang, J., Chae, S.W., Yoo, J., Han, W.G., Hwang, G.H., Jung, J.Y., Choi, J., Jung, H.H., Chung, A.Y., Park, H.C., Choi, J.
ID
ZDB-PUB-140602-1
Date
2014
Source
International journal of pediatric otorhinolaryngology   78(8): 1311-5 (Journal)
Registered Authors
Chung, Ah-Young
Keywords
Caffeic acid phenethyl ester, Neomycin, Ototoxicity, Zebrafish
MeSH Terms
  • Animals
  • Anti-Bacterial Agents/toxicity*
  • Antioxidants/pharmacology*
  • Apoptosis/drug effects
  • Caffeic Acids/pharmacology*
  • Hair Cells, Auditory/drug effects*
  • Hair Cells, Auditory/pathology
  • Microscopy, Electron, Scanning
  • Mitochondria/drug effects
  • Mitochondria/pathology
  • Models, Animal
  • Neomycin/toxicity*
  • Phenylethyl Alcohol/analogs & derivatives*
  • Phenylethyl Alcohol/pharmacology
  • Zebrafish
PubMed
24880922 Full text @ Int. J. Pediatr. Otorhinolaryngol.
Abstract
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).
Five-day post-fertilization zebrafish larvae (n=10) were exposed to 125 μM neomycin and one of the following CAPE concentrations for 1h: 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.
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.
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.
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Human Disease / Model
Sequence Targeting Reagents
Fish
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