title: Photobiomodulation protects the retina from light-induced photoreceptor degeneration.
abstract: OBJECTIVE
  In this study, the hypothesis that near-infrared (NIR) light treatment (photobiomodulation) attenuates bright-light damage in the albino rat retina was tested.
  
  
  METHODS
  Young adult Sprague-Dawley (SD) albino rats were raised in dim (5 lux), cyclic light and then exposed to bright (1000 lux), continuous light for 24 hours. The animals were treated with 670-nm light (9 J/cm(2)) in an LED array before, during, or after exposure to light. The retinas were examined for function, structural changes, cell loss, and markers of stress and inflammation at 1 week and 1 month after exposure to damaging white light.
  
  
  RESULTS
  Bright light caused photoreceptor-specific cell death in control retinas. Significant upregulation of stress and neuroprotective factors and the presence of activated microglia were also noted after light-induced damage. Photobiomodulation profoundly attenuated histopathologic alterations in all three treatment groups. NIR treatment also abolished microglial invasion of the retina and significantly reduced the presence of stress and neuroprotectant molecules. Bright-light-induced reductions in photoreceptor function were significantly ameliorated by photobiomodulation in animals treated before and during exposure to damaging light. Photoreceptor function was initially reduced in animals treated after bright-light-induced damage, but recovered by 1 month after exposure.
  
  
  CONCLUSIONS
  NIR photobiomodulation is protective against bright-light-induced retinal degeneration, even when NIR treatment is applied after exposure to light. This protective effect appears to involve a reduction of cell death and inflammation. Photobiomodulation has the potential to become an important treatment modality for the prevention or treatment of light-induced stress in the retina. More generally, it could be beneficial in the prevention and treatment of retinal conditions involving inflammatory mechanisms.
authors.affiliation: Research School of Biology, National University, Canberra, Australia.
authors.forename: Rizalyn
authors.initials: R
authors.lastname: Albarracin
authors.forename: Janis
authors.initials: J
authors.lastname: Eells
authors.forename: Krisztina
authors.initials: K
authors.lastname: Valter
mesh_terms: D000818:Animals; D002135:Calcium-Binding Proteins / Q000378:metabolism; D020934:Ciliary Neurotrophic Factor / Q000378:metabolism; D004596:Electroretinography; D016222:Fibroblast Growth Factor 2 / Q000235:genetics / Q000378:metabolism; D019084:Fluorescent Antibody Technique, Indirect; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D056747:Immunomodulation; D007259:Infrared Rays; D008027:Light / Q000009:adverse effects*; D008840:Microfilament Proteins / Q000378:metabolism; D010789:Phototherapy; D011833:Radiation Injuries, Experimental / Q000209:etiology / Q000378:metabolism / Q000628:therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000378:metabolism / Q000528:radiation effects*; D012162:Retinal Degeneration / Q000209:etiology / Q000378:metabolism / Q000628:therapy*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013312:Stress, Physiological
chemical_list: C100745:Aif1 protein, rat; D002135:Calcium-Binding Proteins; D020934:Ciliary Neurotrophic Factor; D005904:Glial Fibrillary Acidic Protein; D008840:Microfilament Proteins; D016222:Fibroblast Growth Factor 2