Near-Infrared Photobiomodulation in an Animal Model of Traumatic Brain Injury: Improvements at the Behavioral and Biochemical Levels

Abstract

The purpose of this was to evaluate the neuroprotective effects of near-infrared (NIR) light using an in-vivo rodent model of traumatic brain injury (TBI), controlled cortical impact (CCI), and to characterize changes at the behavioral and biochemical levels. NIR upregulates mitochondrial function, and decreases oxidative stress. Mitochondrial oxidative stress and apoptosis are important in TBI. NIR enhanced cell viability and mitochondrial function in previous in-vitro TBI models, supporting potential NIR in-vivo benefits. Sprague-Dawley rats were divided into three groups: severe TBI, sham surgery, and anesthetization only (behavioral response only). Cohorts in each group were administered either no NIR or NIR. They received two 670 nm LED treatments (5 min, 50 mW/cm(2), 15 J/cm(2)) per day for 72 h (chemical analysis) or 10 days (behavioral). During the recovery period, animals were tested for locomotor and behavioral activities using a TruScan device. Frozen brain tissue was obtained at 72 h and evaluated for apoptotic markers and reduced glutathione (GSH) levels. Significant differences were seen in the TBI plus and minus NIR (TBI+/-) and sham plus and minus NIR (S+/-) comparisons for some of the TruScan nose poke parameters. A statistically significant decrease was found in the Bax pro-apoptotic marker attributable to NIR exposure, along with lesser increases in Bcl-2 anti-apoptotic marker and GSH levels. These results show statistically significant, preclinical outcomes that support the use of NIR treatment after TBI in effecting changes at the behavioral, cellular, and chemical levels.