670nm photobiomodulation modulates bioenergetics and oxidative stress, in rat Müller cells challenged with high glucose

• Published in: PloS one Vol. 16; no. 12; p. e0260968
• Main Authors: Nonarath, Hannah J, Hall, Alexandria E, SenthilKumar, Gopika, Abroe, Betsy, Eells, Janis T, Liedhegner, Elizabeth S
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 03.12.2021; Public Library of Science (PLoS)
• Subjects: Animals; Apoptosis; Bioenergetics; Biology and Life Sciences; Care and treatment; Cell culture; Cells, Cultured; Clinical trials; Diabetes; Diabetes mellitus; Diabetic retinopathy; Energy Metabolism; Ependymoglial Cells - drug effects; Ependymoglial Cells - pathology; Ependymoglial Cells - radiation effects; Glial cells; Glucose; Glucose - toxicity; Growth factors; Health aspects; Health sciences; Inflammation; Infrared radiation; Infrared Rays; Intercellular adhesion molecule 1; Light emitting diodes; Light therapy; Medicine and Health Sciences; Methods; Mitigation; Mitochondria; Mitochondria - drug effects; Mitochondria - pathology; Mitochondria - radiation effects; Mueller cells; Neurosciences; NF-κB protein; Oxidative Stress; Oxygen; Phenols; Phototherapy; Physical Sciences; Rats; Reactive oxygen species; Reactive Oxygen Species - metabolism; Research and analysis methods; Retina; Retinopathy; Sweetening Agents - toxicity; Testing; Vascular endothelial growth factor; United States; United States > US; Wisconsin
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0260968

Diabetic retinopathy (DR), the most common complication of diabetes mellitus, is associated with oxidative stress, nuclear factor-κB (NFκB) activation, and excess production of vascular endothelial growth factor (VEGF) and intracellular adhesion molecule-1 (ICAM-1). Muller glial cells, spanning the entirety of the retina, are involved in DR inflammation. Mitigation of DR pathology currently occurs via invasive, frequently ineffective therapies which can cause adverse effects. The application of far-red to near-infrared (NIR) light (630-1000nm) reduces oxidative stress and inflammation in vitro and in vivo. Thus, we hypothesize that 670nm light treatment will diminish oxidative stress preventing downstream inflammatory mechanisms associated with DR initiated by Muller cells. In this study, we used an in vitro model system of rat Müller glial cells grown under normal (5 mM) or high (25 mM) glucose conditions and treated with a 670 nm light emitting diode array (LED) (4.5 J/cm2) or no light (sham) daily. We report that a single 670 nm light treatment diminished reactive oxygen species (ROS) production and preserved mitochondrial integrity in this in vitro model of early DR. Furthermore, treatment for 3 days in culture reduced NFκB activity to levels observed in normal glucose and prevented the subsequent increase in ICAM-1. The ability of 670nm light treatment to prevent early molecular changes in this in vitro high glucose model system suggests light treatment could mitigate early deleterious effects modulating inflammatory signaling and diminishing oxidative stress.