Low-level laser facilitates alternatively activated macrophage/microglia polarization and promotes functional recovery after crush spinal cord injury in rats

Sci Rep. 2017 Apr 4;7(1):620. doi: 10.1038/s41598-017-00553-6.


Macrophages and resident microglia play an import role in the secondary neuroinflammation response following spinal cord injury. Reprogramming of macrophage/microglia polarization is an import strategy for spinal cord injury restoration. Low-level laser therapy (LLLT) is a noninvasive treatment that has been widely used in neurotrauma and neurodegenerative diseases. However, the influence of low-level laser on polarization of macrophage/microglia following spinal cord injury remains unknown. The present study applied low-level laser therapy on a crush spinal cord injury rat model. Using immunofluorescence, flow cytometry, RT-qPCR, and western blot assays, we found that low-level laser therapy altered the polarization state to a M2 tendency. A greater number of neurons survived in the pare injury site, which was accompanied by higher BBB scores in the LLLT group. Furthermore, low-level laser therapy elevated expression of interleukin 4 (IL-4) and interleukin 13 (IL-13). Results from this study show that low-level laser therapy has the potential for reducing inflammation, regulating macrophage/microglia polarization, and promoting neuronal survival. These beneficial effects demonstrate that low-level laser therapy may be an effective candidate for clinical treatment of spinal cord injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / metabolism
  • Behavior, Animal
  • Biomarkers
  • Cytokines / metabolism
  • Disease Models, Animal
  • Inflammation Mediators / metabolism
  • Laser Therapy* / methods
  • Macrophage Activation / immunology*
  • Macrophages / immunology
  • Macrophages / metabolism*
  • Microglia / metabolism*
  • Neurons / metabolism
  • Neuroprotection
  • Phenotype
  • Rats
  • Recovery of Function / radiation effects*
  • Spinal Cord Injuries / etiology
  • Spinal Cord Injuries / metabolism*
  • Spinal Cord Injuries / rehabilitation*
  • Spinal Cord Injuries / therapy


  • Biomarkers
  • Cytokines
  • Inflammation Mediators