Effect of low level laser therapy on chronic compression of the dorsal root ganglion

PLoS One. 2014 Mar 4;9(3):e89894. doi: 10.1371/journal.pone.0089894. eCollection 2014.


Dorsal root ganglia (DRG) are vulnerable to physical injury of the intervertebral foramen, and chronic compression of the DRG (CCD) an result in nerve root damage with persistent morbidity. The purpose of this study was to evaluate the effects of low level laser therapy (LLLT) on the DRG in a CCD model and to determine the mechanisms underlying these effects. CCD rats had L-shaped stainless-steel rods inserted into the fourth and fifth lumbar intervertebral foramen, and the rats were then subjected to 0 or 8 J/cm2 LLLT for 8 consecutive days following CCD surgery. Pain and heat stimuli were applied to test for hyperalgesia following CCD. The levels of TNF-α, IL-1β and growth-associated protein-43 (GAP-43) messenger RNA (mRNA) expression were measured via real-time PCR, and protein expression levels were analyzed through immunohistochemical analyses. Our data indicate that LLLT significantly decreased the tolerable sensitivity to pain and heat stimuli in the CCD groups. The expression levels of the pro-inflammatory cytokines TNF-α and IL-1β were increased following CCD, and we found that these increases could be reduced by the application of LLLT. Furthermore, the expression of GAP-43 was enhanced by LLLT. In conclusion, LLLT was able to enhance neural regeneration in rats following CCD and improve rat ambulatory behavior. The therapeutic effects of LLLT on the DRG during CCD may be exerted through suppression of the inflammatory response and induction of neuronal repair genes. These results suggest potential clinical applications for LLLT in the treatment of compression-induced neuronal disorders.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • GAP-43 Protein / metabolism
  • Ganglia, Spinal / diagnostic imaging
  • Ganglia, Spinal / pathology*
  • Gene Expression Regulation
  • Hyperalgesia / etiology
  • Hyperalgesia / radiotherapy
  • Inflammation Mediators / metabolism
  • Low-Level Light Therapy*
  • Male
  • Nerve Compression Syndromes / complications
  • Nerve Compression Syndromes / diagnostic imaging
  • Nerve Compression Syndromes / genetics
  • Nerve Compression Syndromes / radiotherapy*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Radiography
  • Rats, Sprague-Dawley
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism


  • GAP-43 Protein
  • Inflammation Mediators
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha

Grants and funding

This study was supported by a grant from the National Health Research Institutes (NHRI-EX 102-9914EC), a grant from the National Science Council (NSC97-2314-B-037-004-MY3) and grants from the Kaohsiung Medical University (KMU-Q098007, KMU-Q098025 and KMU-Q099018). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.