Effect of 670 nm Photobiomodulation on Retinal Function & Energy Metabolism in Aging Mice

Metabolic dysfunction is a common hallmark of aging. Recent studies have established the metabolic footprint of aging in the mouse. Aging has been shown to reduce retinal function and modify mitochondrial metabolism and redox homeostasis. Photobiomodulation (PBM) with far-red to near infrared (NIR) light has been demonstrated to improve/restore mitochondrial function and improve redox homeostasis in mammalian and drosophila models of aging. We tested the hypothesis that PBM would protect against the loss of retinal function and modify the metabolic footprint of aging in C57/BL mice. Experiments were conducted in 12-month old C57BL/6 mice. Baseline full-flash electroretinograms (ERGs) were recorded and animals were divided into two treatment groups: PBM and Sham. Mice were treated daily for 4 weeks with 670 nm light at a dose of 4.5 J/cm2. Sham treated animals were restrained, but not exposed to 670 nm light. Mice were euthanized following the recording of post-treatment ERGs. Tissues (retina, brain, liver, kidney and skeletal muscle) were harvested, flash-frozen in liquid nitrogen at stored at -80C until analyzed for metabolites. The difference between post-treatment and baseline ERG b-wave responses at 10,000 mcds/m2 in sham treated animals was -191 µV. In PBM-treated animals it was -72 µV. These data indicate that 670 nm PBM protects against the loss of retinal function in aged C57BL/6. We have begun to analyze the effect of PBM on metabolites reported to be significantly depleted in aged tissues in the C57/BL mouse including cytochrome c-oxidase, transcription factor A (TFAM), and Bax. This study was designed to improve our understanding of PBM on metabolic aging. Moreover, the identification of biomarkers of aging may spur the rational design of strategies to attenuate the decline in key metabolic networks and prevent accelerated aging