Blue light reduces organ injury from ischemia and reperfusion

Would wearing blue light googles immediately upon entering the ambulance or hospital prevent some of the reperfusion injury? We'll never know because we have NO leadership and NO strategy in stroke.

Blue light reduces organ injury from ischemia and reperfusion

Du Yuan,^a,b,1 Richard D. Collage,^a,1 Hai Huang,^a Xianghong Zhang,^a Benjamin C. Kautza,^a Anthony J. Lewis,^a Brian S. Zuckerbraun,^a Allan Tsung,^a Derek C. Angus,^c and Matthew R. Rosengart^a,c,2

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Significance

It is well established that light regulates mammalian biology. And yet, we have been unable to define and thus harness the underlying mechanisms so as to apply them to alter the course of human disease. In this study we determine that the spectrum of light is a critical determinant of its effect on critical illness. We show that an acute and short (24 h) exposure to high-illuminance (1,400 lx) blue spectrum (peak 442 nm) light prior to ischemia/reperfusion (I/R) significantly attenuates the degree of organ injury. Our characterization of the biological mechanisms through which blue light beneficially alters the cellular response to I/R provides an opportunity to develop novel therapeutics for the prevention and treatment of many diseases.

Keywords: blue light, ischemia, reperfusion, organ injury, circadian rhythms

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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.