Effects of low-level laser therapy (GaAs) in an animal model of muscular damage induced by trauma.

It has been demonstrated that reactive oxygen species (ROS) formation and oxidative damage markers are increased after muscle damage. Recent studies have demonstrated that low-level laser therapy (LLLT) modulates many biochemical processes mainly those related to reduction of muscular injures, increment of mitochondrial respiration and ATP synthesis, as well as acceleration of the healing process. The objective of the present investigation was to verify the influence of LLLT in some parameters of muscular injury, oxidative damage, antioxidant activity, and synthesis of collagen after traumatic muscular injury. Adult male Wistar rats were divided randomly into three groups (n = 6), namely, sham (uninjured muscle), muscle injury without treatment, and muscle injury with LLLT (GaAs, 904 nm). Each treated point received 5 J/cm(2) or 0.5 J of energy density (12.5 s) and 2.5 J per treatment (five regions). LLLT was administered 2, 12, 24, 48, 72, 96, and 120 h after muscle trauma. The serum creatine kinase activity was used as an index of skeletal muscle injury. Superoxide anion, thiobarbituric acid reactive substance (TBARS) measurement, and superoxide dismutase (SOD) activity were used as indicators of oxidative stress. In order to assess the synthesis of collagen, levels of hydroxyproline were measured. Our results have shown that the model of traumatic injury induces a significant increase in serum creatine kinase activity, hydroxyproline content, superoxide anion production, TBARS level, and activity of SOD compared to control. LLLT accelerated the muscular healing by significantly decreasing superoxide anion production, TBARS levels, the activity of SOD, and hydroxyproline content. The data strongly indicate that increased ROS production and augmented collagen synthesis are elicited by traumatic muscular injury, effects that were significantly decreased by LLLT.