Research reportPhotobiomodulation rescues the cochlea from noise-induced hearing loss via upregulating nuclear factor κB expression in rats

- ABR measurement revealed that PBM accelerated recovery of auditory function.
- Immunoreactivities against iNOS and cleaved-caspase 3 decreased with PBM in the outer hair cells.
- Immunoreactivities against NF-κB increased with PBM in the lateral wall and the spiral ganglion cells.
- Western blot showed increased NF-κB activation after PBM.

Photobiomodulation (PBM) is a noninvasive treatment that can be neuroprotective, although the underlying mechanisms remain unclear. In the present study, we assessed the mechanism of PBM as a novel treatment for noise-induced hearing loss, focusing on the nuclear factor (NF)-κB signaling pathway. Sprague-Dawley rats were exposed to 1-octave band noise centered at 4 kHz for 5 h (121 dB). After noise exposure, their right ears were irradiated with an 808 nm diode laser beam at an output power density of 165 mW/cm2 for 30 min a day for 5 consecutive days. Measurement of the auditory brainstem response revealed an accelerated recovery of auditory function in the groups treated with PBM compared with the non-treatment group at 4, 7, and 14 days after noise exposure. Immunofluorescent image analysis for inducible nitric oxide synthase and cleaved caspase-3 showed lesser immunoreactivities in outer hair cells in the PBM group compared with the non-treatment group. However, immunofluorescent image analysis for NF-κB, an upstream protein of inducible nitric oxide synthase, revealed greater activation in the PBM group compared with the naïve and non-treatment groups. Western blot analysis for NF-κB also showed stronger activation in the cochlear tissues in the PBM group compared with the naïve and non-treatment groups (p<0.01, each). These data suggest that PBM activates NF-κB to induce protection against inducible nitric oxide synthase-triggered oxidative stress and caspase-3-mediated apoptosis that occur following noise-induced hearing loss.