Effects of low-level laser therapy (LLLT) on the nuclear factor (NF)-kappaB signaling pathway in traumatized muscle

• Published in: Lasers in surgery and medicine Vol. 38; no. 7; pp. 704 - 713
• Main Authors: Rizzi, Carem Fetter, Mauriz, José Luis, Freitas Corrêa, Daniela Sousa, Moreira, Andréa Janz, Zettler, Claudio Galeano, Filippin, Lidiane Isabel, Marroni, Norma Possa, González-Gallego, Javier
• Format: Journal Article
• Language: English
• Published: United States 01-08-2006
• Subjects: Animals; Arsenic; Collagen - analysis; Collagen - radiation effects; Disease Models, Animal; Gallium; Lasers; Low-Level Light Therapy - instrumentation; Male; Muscle, Skeletal - injuries; Muscle, Skeletal - pathology; Muscle, Skeletal - radiation effects; NF-kappa B - radiation effects; Nitric Oxide Synthase Type II - radiation effects; Oxidative Stress - radiation effects; Random Allocation; Rats; Rats, Wistar; Reactive Oxygen Species - radiation effects; Signal Transduction - radiation effects; Time Factors; Up-Regulation - radiation effects; Wounds, Nonpenetrating - radiotherapy
• ISSN: 0196-8092

To investigate the effects of low-level laser therapy (LLLT) on nuclear factor kappa B (NF-kappaB) activation and inducible nitric oxide synthase (iNOS) expression in an experimental model of muscle trauma.
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/cm2) was applied for 35 seconds duration, continuously.
Histological abnormalities with increase in collagen concentration, and oxidative stress were observed after trauma. This was accompanied by activation of NF-kappaB and upregulation of iNOS expression, whereas protein concentration of I kappa B alpha decreased. These effects were blocked by LLLT.
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-kappaB. The associated reduction of iNOS overexpression and collagen production suggest that the NF-kappaB pathway may be a signaling route involved in the pathogenesis of muscle trauma.