Low-level laser therapy attenuates the acute inflammatory response induced by muscle traumatic injury.

The purpose of this work was to investigate the effect of early and long-term low-level laser therapy (LLLT) on oxidative stress and inflammatory biomarkers after acute-traumatic muscle injury in Wistar rats. Animals were randomly divided into the following four groups: control group (CG), muscle injury group (IG), CG + LLLT, and IG + LLLT: laser treatment with doses of 3 and 5 J/cm(2). Muscle traumatic injury was induced by a single-impact blunt trauma in the rat gastrocnemius. Irradiation for 3 or 5 J/cm(2) was initiated 2, 12, and 24 h after muscle trauma induction, and the treatment was continued for five consecutive days. All the oxidant markers investigated. namely thiobarbituric acid-reactive substance, carbonyl, superoxide dismutase, glutathione peroxidase, and catalase, were increased as soon as 2 h after muscle injury and remained increased up to 24 h. These alterations were prevented by LLLT at a 3 J/cm(2) dose given 2 h after the trauma. Similarly, LLLT prevented the trauma-induced proinflammatory state characterized by IL-6 and IL-10. In parallel, trauma-induced reduction in BDNF and VEGF, vascular remodeling and fiber-proliferating markers, was prevented by laser irradiation. In order to test whether the preventive effect of LLLT was also reflected in muscle functionality, we tested the locomotor activity, by measuring distance traveled and the number of rearings in the open field test. LLLT was effective in recovering the normal locomotion, indicating that the irradiation induced biostimulatory effects that accelerated or resolved the acute inflammatory response as well as the oxidant state elicited by the muscle trauma.

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.