Abstract Title:

Low level laser therapy alters satellite glial cell expression and reverses nociceptive behavior in rats with neuropathic pain.

Abstract Source:

Photochem Photobiol Sci. 2017 Jan 26. Epub 2017 Jan 26. PMID: 28125108

Abstract Author(s):

M E Oliveira, F M Santos, R P Bonifácio, M F Freitas, D O Martins, M Chacur

Article Affiliation:

M E Oliveira


BACKGROUND: Nerve injury often results in persistent or chronic neuropathic pain characterized by spontaneous burning pain accompanied by allodynia and hyperalgesia. Low level laser therapy (LLLT) is a noninvasive method that has proved to be clinically effective in reducing pain sensitivity and consequently in improving the quality of life. Here we examined the effects of LLLT on pain sensitivity induced by chronic constriction injury (CCI) in rats. CCI was performed on adult male rats, subjected thereafter to 10 sessions of LLLT, every other day, and starting 14 days after CCI. Over the treatment period, the animals were evaluated for nociception using behavioral tests, such as allodynia, thermal and mechanical hyperalgesia. Following the sessions, we observed the involvement of satellite glial cells in the dorsal root ganglion (DRG) using immunoblotting and immunofluorescence approaches. In addition we analyzed the expression levels of interleukin 1 (IL-1β) and fractalkine (FKN) after the same stimulus.

RESULTS: LLLT induced an early reduction (starting at the second session; p≤ 0.001) of the mechanical and thermal hyperalgesia and allodynia in CCI rats, which persisted until the last session. Regarding cellular changes, we observed a decrease of GFAP (50%; p ≤ 0.001) expression after LLLT in the ipsilateral DRG when compared with the naive group. We also observed a significant increase of pro-inflammatory cytokines after CCI, whereas LLLT dramatically inhibited the overexpression of these proteins.

CONCLUSIONS: These data provide evidence that LLLT reverses CCI-induced behavioral hypersensitivity, reduces glial cell activation in the DRG and decreases pro-inflammatory cytokines; we suggest that this involvement of glial cells can be one potential mechanism in such an effect.

Study Type : Animal Study

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