Histomorphologic and ultrastructural recovery of myopathy in rats treated with low-level laser therapy.

The purpose of the present work was to study the effect of low-level laser therapy (LLLT): helium-neon (He-Ne) and gallium arsenide (Ga-As) laser on the histomorphology of muscle and mitochondria in experimental myopathy in rats. Thirty Suquía strain female rats were distributed in groups: (A) control (intact), (B) injured, (C) injured and treated with He-Ne laser, (D) injured and treated with Ga-As laser, (E) irradiated with He-Ne laser on the non-injured muscle, and (F) irradiated with Ga-As laser on the non-injured muscle. Myopathy was induced by injecting 0.05 mg/rat/day of adrenaline in the left gastrocnemius muscle at the same point on five consecutive days, in groups B, C, and D. LLLT was applied with 9.5 J cm-2 daily for seven consecutive days in groups C, D, E, and F. The muscles were examined with optic and electronic microscopy. The inflammation was classified as absent, mild, and intense and the degree of mitochondrial alteration was graded I, II, III, and IV. Categorical data were statistically analyzed by Chi-square and the Fisher-Irwin Bilateral test, setting significant difference at p < 0.05. The damage found in muscle and mitochondria histomorphology in animals with induced myopathy (B) was intense or severe inflammation with grade III or IV of mitochondrial alteration. They underwent significant regression (p < 0.001) compared with the groups treated with He-Ne (C) and Ga-As (D) laser, in which mild or moderate inflammation was seen and mitochondrial alteration grades I and II, recovering normal myofibrillar architecture. No differences were found between the effects caused by the two lasers, or between groups A, E, and F. Group A was found to be different from B, C, and D (p < 0.001). LLLT in experimental myopathy caused significant muscular and mitochondrial morphologic recovery.

Evaluation of inflammatory biomarkers associated with oxidative stress and histological assessment of magnetic therapy on experimental myopathy in rats.

The effect of pulsed electromagnetic field (PEMF) therapy, also called magnetic therapy, upon inflammatory biomarkers associated with oxidative stress plasma fibrinogen, nitric oxide (NO), L-citrulline, carbonyl groups, and superoxide dismutase (SOD) was evaluated through histological assessment, in rats with experimental myopathy. The groups studied were: (A) control (intact rats that received PEMF sham exposures); (B) rats with myopathy and sacrificed 24 h later; (C) rats with myopathy; (D) rats with myopathy and treated with PEMF; and (E) intact rats treated with PEMF. Groups A, C, D, and E were sacrificed 8 days later. Myopathy was induced by injecting 50 µl of 1% carrageenan λ (type IV) once sub-plantar. Treatment was carried out with PEMF emitting equipment with two flat solenoid disks for 8 consecutive days in groups D and E, at 20 mT and 50 Hz for 30 min/day/rat. The biomarkers were determined by spectrophotometry. The muscles (5/8) were stained with Hematoxylin-Eosin and examined by optic microscopy. Quantitative variables were statistically analyzed by the Fisher test, and categorical applying Pearson's Chi Squared test at p < 0.05 for all cases. In Groups B and C, the biomarkers were significantly increased compared to A, D, and E groups: fibrinogen (p < 0.001); NO, L-citrulline and carbonyl groups (p < 0.05); SOD (p < 0.01) as well as the percentage of area with inflammatory infiltration (p < 0.001). PEMF caused decreased levels of fibrinogen, L-citrulline, NO, SOD, and carbonyl groups and significant muscle recovery in rats with experimental myopathies.

Low level laser therapy on experimental myopathy.

PURPOSE: The aim of the present work was to study the effect of Helium-Neon (HeNe) and Gallium Arsenide (GaAs) laser upon nitric oxide (NO) plasma levels, an inflammatory biomarker associated with oxidative stress, in rats with experimental myopathy. These were evaluated through histological assessment. MATERIALS AND METHODS: The groups studied were: (A) control (intact rats that received LLLT sham exposures), (B) rats with myopathy and sacrificed at 24 h later, (C) rats with myopathy and sacrificed 8 days later, (D) rats with myopathy and treated with HeNe laser, (E) rats with myopathy and treated with GaAs laser, (F) intact rats treated with HeNe laser and (G) intact rats treated with GaAs laser. Myopathy was induced by injecting 50µl of 1% carrageenan λ (type IV) in the left gastrocnemius muscle. Low Level Laser Therapy (LLLT) was applied with 9.5 J.cm(-2) daily for 10 consecutive days with each laser. The determination of the NO was made by spectrophotometry. The muscles were stained with Hematoxylin-Eosin and examined by optic microscopy. Quantitative variables were statistically analyzed by the Fisher test, and categorical by applying Pearson's Chi Squared test at p <0.05 for all cases. RESULTS: In groups B and C, NO was significantly increased compared to groups A, D, E, F and G (p<0.05). In group C, the percentage of area with inflammatory infiltration was significantly increased compared to the other groups (p<0.001). CONCLUSIONS: LLLT decreased plasma levels of NO in rats with experimental myopathies and significant muscle recovery.

Evaluation of inflammatory biomarkers associated with oxidative stress and histological assessment of low-level laser therapy in experimental myopathy.

UNLABELLED: The objective of the present work was to study the effect of helium-neon (He-Ne) and gallium-arsenide (Ga-As) laser upon inflammatory biomarkers associated with oxidative stress: fibrinogen, nitric oxide (NO), L-citrulline, and superoxide dismutase (SOD). These were evaluated through histological assessment, in rats with experimental myopathy. MATERIALS AND METHODS: The groups studied were: (A) control, (B) injured, (C) injured and treated with He-Ne laser, (D) injured and treated with Ga-As laser, (E) irradiated with He-Ne; and (F) irradiated with Ga-As laser. Myopathy was induced by injecting 0.05 mg/rat/day of adrenaline in the left posterior limb muscle at the same point on 5 consecutive days, in groups B, C, and D. Low-level laser therapy (LLLT) was applied with 9.5 J/cm(2) daily for 7 consecutive days with each laser. The determination of the biomarkers was made by spectrophotometry. The muscles (5/8, single blinded) were stained with Gomori Trichrome and examined by optic microscopy. The quantitative variables were statistically analyzed by the Fisher's test and categorical data by the Axionvision 4.8 program. Pearson's chi-squared test was applied, setting significant difference at P < 0.05 for all cases. RESULTS: In group B, the biomarkers were significantly increased compared to the other groups (P < 0.001), except for NO which in group B decreased significantly (P < 0.001). In group B, there was a higher inflammatory infiltration level (80.67%) in relation to destroyed fibers. CONCLUSIONS: LLLT caused significant changes in inflammatory biomarkers and oxidative stress: decreased levels of fibrinogen, L-citrulline and SOD as opposed to the increase of NO in rats with experimental myopathies and significant muscle recovery.

Laser therapy on arthritis induced by urate crystals.

OBJECTIVE: We aimed to evaluate low-power laser therapy efficacy on fibrinogen (PF) in the plasma of rats with arthritis induced by urate crystals. In addition, anatomopathological (AP) studies were carried out. BACKGROUND DATA: Raised blood uric acid may form microscopic crystals in the joint. These crystals set up the inflammation called "acute gouty arthritis." METHODS: Two mg of uric acid were injected in both joints of the lower limbs of rats over 2 days. A group was treated with He-Ne laser (6 mW) on the injected joints during 3 consecutive days. After 96 h of the first injection, animals were sacrificed to determine fibrinogen by spectrophotometry. Sections from the lower limbs were used for AP studies. RESULTS: A statistically significant increase (p < 0.001) in plasma fibrinogen levels was observed in the group injected with urates, when compared to both control group and the laser-treated group. The AP observed in the untreated group showed an intense fibroblastic proliferation and chronic inflammation. In the group treated with laser no inflammatory reaction was observed. CONCLUSIONS: Laser therapy has an anti-inflammatory effect in arthropathy induced in rats injected with urates, determined by fibrinogen levels and by histological involution.