Blue light reduces organ injury from ischemia and reperfusion

Proc Natl Acad Sci U S A. 2016 May 10;113(19):5239-44. doi: 10.1073/pnas.1515296113. Epub 2016 Apr 25.

Abstract

Evidence suggests that light and circadian rhythms profoundly influence the physiologic capacity with which an organism responds to stress. However, the ramifications of light spectrum on the course of critical illness remain to be determined. Here, we show that acute exposure to bright blue spectrum light reduces organ injury by comparison with bright red spectrum or ambient white fluorescent light in two murine models of sterile insult: warm liver ischemia/reperfusion (I/R) and unilateral renal I/R. Exposure to bright blue light before I/R reduced hepatocellular injury and necrosis and reduced acute kidney injury and necrosis. In both models, blue light reduced neutrophil influx, as evidenced by reduced myeloperoxidase (MPO) within each organ, and reduced the release of high-mobility group box 1 (HMGB1), a neutrophil chemotactant and key mediator in the pathogenesis of I/R injury. The protective mechanism appeared to involve an optic pathway and was mediated, in part, by a sympathetic (β3 adrenergic) pathway that functioned independent of significant alterations in melatonin or corticosterone concentrations to regulate neutrophil recruitment. These data suggest that modifying the spectrum of light may offer therapeutic utility in sterile forms of cellular injury.

Keywords: blue light; circadian rhythms; ischemia; organ injury; reperfusion.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Color Therapy / methods*
  • Color*
  • Corticosterone / blood*
  • Dose-Response Relationship, Radiation
  • HMGB1 Protein / blood
  • Kidney Function Tests
  • Liver Function Tests
  • Male
  • Melatonin / blood
  • Mice
  • Mice, Inbred C57BL
  • Peroxidase / blood
  • Radiation Dosage
  • Reperfusion Injury / diagnosis
  • Reperfusion Injury / physiopathology*
  • Reperfusion Injury / prevention & control*
  • Severity of Illness Index
  • Treatment Outcome

Substances

  • HMGB1 Protein
  • HMGB1 protein, mouse
  • Peroxidase
  • Melatonin
  • Corticosterone