Recent studies have demonstrated that excessive oxidative stress in the cochlea is closely related to the pathogenesis of both NIHL and AHL, implying that appropriate control of oxidative stress is an effective strategy to prevent the development and progression of the majority of SNHL cases in adulthood. Noise-induced hearing loss (NIHL) and age-related hearing loss (AHL) are two major classes of sensorineural hearing loss (SNHL) in adult populations. Thus, high NRF2 activity is advantageous for cochlear protection from noise-induced injury and NRF2 is a promising target for NIHL prevention. Consistently, a human NRF2 SNP was significantly associated with impaired sensorineural hearing levels in a cohort subjected to occupational noise exposure. Therefore, NRF2 activation is effective for NIHL prevention. Treatment with CDDO-Im, a potent NRF2-activating drug, before but not after the noise exposure preserved the integrity of hair cells and improved post-exposure hearing levels in wild-type mice, but not in Nrf2 –/– mice. Threshold shifts of the auditory brainstem response at 7 days post-exposure were significantly larger in Nrf2 –/– mice than wild-type mice. To clarify the contribution of NRF2 to cochlear protection, we examined Nrf2 –/– mice for susceptibility to NIHL.
#Agilent chemstation noise ptop Activator#
NRF2 is a transcriptional activator playing an essential role in the defense mechanism against oxidative stress. This suggests that protecting the cochlea from oxidative stress is an effective therapeutic approach for NIHL.
#Agilent chemstation noise ptop free#
Recent studies have demonstrated that the pathogenesis of NIHL is closely related to ischemia-reperfusion injury of cochlea, which is caused by blood flow decrease and free radical production due to excessive noise. Noise-induced hearing loss (NIHL) is one of the most common sensorineural hearing deficits.
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