• DOI:10.1002/jbio.201500209
• Corpus ID: 30144922

Pre-conditioning with near infrared photobiomodulation reduces inflammatory cytokines and markers of oxidative stress in cochlear hair cells.

@article{Bartos2016PreconditioningWN,
  title={Pre-conditioning with near infrared photobiomodulation reduces inflammatory cytokines and markers of oxidative stress in cochlear hair cells.},
  author={Adam Bartos and Yohann Grondin and Magda E. Bortoni and Elisa Ghelfi and Rosalinda Sep{\'u}lveda Sep{\'u}lveda and James Carroll and Rick A. Rogers},
  journal={Journal of biophotonics},
  year={2016},
  volume={9 11-12},
  pages={
          1125-1135
        }
}

• Adam Bartos, Y. Grondin, +4 authors Rick A. Rogers
• Published 1 December 2016
• Biology
• Journal of biophotonics

Hearing loss is a serious occupational health problem worldwide. Noise, aminoglycoside antibiotics and chemotherapeutic drugs induce hearing loss through changes in metabolic functions resulting in sensory cell death in the cochlea. Metabolic sequelae from noise exposure increase production of nitric oxide (NO) and Reactive Oxygen Species (ROS) contributing to higher levels of oxidative stress beyond the physiologic threshold levels of intracellular repair. Photobiomodulation (PBM) therapy is a light treatment involving endogenous chromophores commonly used to reduce inflammation and promote tissue repair. Near infrared light (NIR) from Light Emitting Diodes (LED) at 810 nm wavelength were used as a biochemical modulator of cytokine response in cultured HEI-OC1 auditory cells placed under oxidative stress. Results reported here show that NIR PBM at 810 nm, 30 mW/cm2 , 100 seconds, 1.0 J, 3 J/cm2 altered mitochondrial metabolism and oxidative stress response for up to 24 hours post treatment. We report a decrease of inflammatory cytokines and stress levels resulting from NIR applied to HEI-OC1 auditory cells before treatment with gentamicin or lipopolysaccharide. These results show that cells pretreated with NIR exhibit reduction of proinflammatory markers that correlate with inhibition of mitochondrial superoxide, ROS and NO in response to continuous oxidative stress challenges. Non-invasive biomolecular down regulation of proinflammatory intracellular metabolic pathways and suppression of oxidative stress via NIR may have the potential to develop novel therapeutic approaches to address noise exposure and ototoxic compounds associated with hearing loss.