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Effects of low‐level laser therapy (LLLT) on the nuclear factor (NF)‐κB signaling pathway in traumatized muscle
Author(s) -
Rizzi Carem Fetter,
Mauriz José Luis,
Freitas Corrêa Daniela Sousa,
Moreira Andréa Janz,
Zettler Claudio Galeano,
Filippin Lidiane Isabel,
Marroni Norma Possa,
GonzálezGallego Javier
Publication year - 2006
Publication title -
lasers in surgery and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 112
eISSN - 1096-9101
pISSN - 0196-8092
DOI - 10.1002/lsm.20371
Subject(s) - low level laser therapy , downregulation and upregulation , nitric oxide , nitric oxide synthase , oxidative stress , reactive oxygen species , nf κb , pathogenesis , chemistry , inflammation , signal transduction , nfkb1 , endocrinology , medicine , transcription factor , laser therapy , biochemistry , laser , physics , optics , gene
Background and Objective To investigate the effects of low‐level laser therapy (LLLT) on nuclear factor kappa B (NF‐κB) activation and inducible nitric oxide synthase (iNOS) expression in an experimental model of muscle trauma. Study Design/Materials and Methods Injury to the gastrocnemius muscle in the rat was produced by a single impact blunt trauma. A low‐level galium arsenide (Ga–As) laser (904 nm, 45 mW, and 5 J/cm 2 ) was applied for 35 seconds duration, continuously. Results Histological abnormalities with increase in collagen concentration, and oxidative stress were observed after trauma. This was accompanied by activation of NF‐κB and upregulation of iNOS expression, whereas protein concentration of IκBα decreased. These effects were blocked by LLLT. Conclusion LLLT reduced the inflammatory response induced by trauma and was able to block the effects of reactive oxygen species (ROS) release and the activation of NF‐κB. The associated reduction of iNOS overexpression and collagen production suggest that the NF‐κB pathway may be a signaling route involved in the pathogenesis of muscle trauma. Lasers Surg. Med. © 2006 Wiley‐Liss, Inc.