A Peptide Inhibitor of c-Jun N-Terminal Kinase Protects against Both Aminoglycoside and Acoustic Trauma-Induced Auditory Hair Cell Death and Hearing Loss

• DOI: 10.1523/jneurosci.23-24-08596.2003
• Publication Date: 2018-04-12T23:25:04Z
• Authors: J. Wang; T. R. Van De Water; C. Bonny; F. de Ribaupierre; J. L. Puel; A. Zine
• Keywords: Ototoxicity; Neomycin

Hearing loss can be caused by a variety of insults, including acoustic trauma and exposure to ototoxins, that principally effect the viability sensory hair cells via MAP kinase (MAPK) cell death signaling pathway incorporates c-Jun N-terminal (JNK). We evaluated otoprotective efficacy D-JNKI-1, permeable peptide blocks MAPK-JNK signal pathway. The experimental studies included organ cultures neonatal mouse cochlea exposed an ototoxic drug cochleae adult guinea pigs were either or trauma. Results obtained from Corti explants demonstrated is associated with injury blocking this prevented apoptosis in areas aminoglycoside damage. Treatment neomycin-exposed D-JNKI-1 completely initiated ototoxin. vivo showed direct application into scala tympani pig nearly all permanent hearing induced neomycin ototoxicity. Local delivery also trauma-induced dose-dependent manner. These results indicate involved both ototoxicity loss. Blocking potential therapeutic value for long-term protection morphological integrity physiological function during times oxidative stress.