The Injured Cochlea as a Target for Inflammatory Processes, Initiation of Cell Death Pathways and Application of Related Otoprotective Strategies

摘要: One of the causes sensorineural hearing loss is auditory hair cells following exposure to environmental stresses. Auditory cell death in response cochlear trauma occurs via both necrosis and apoptosis. Apoptosis involves caspase MAPK/JNK pathways which are activated by oxidative stress secretion inflammatory cytokines trauma. Identification that lead apoptosis provides therapeutic targets for conservation hearing. Antioxidants reduce level reactive oxygen species nitrogen generated acoustic trauma, aminoglycoside platinum-based drugs. Caspase inhibitors affect extrinsic intrinsic apoptotic thereby reducing cisplatin, aminoglycoside, hydraulic ischemia-induced losses. Corticosteroid therapy reduces inflammation inhibits while activating pro-survival organ Corti noise, vibration, ischemia/reperfusion injury, bacterial meningitis electrode insertion Inhibitors JNK signaling pathway prevent acute labyrinthitis, ototoxicity. This review an overview different involved traditional newly developed drugs currently being studied or used treatment loss. Recent patents related otoprotective strategies conserve also discussed this review.