Juan Carlos Simes

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

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/cm2 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 Fishers test and categorical data by the Axionvision 4.8 program. Pearsons 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. Lasers Surg. Med. 42:577–583, 2010.

Inflammatory and oxidative stress markers in experimental crystalopathy: their modification by photostimulation.

Crystalopathies are inflammatory pathologies caused by cellular reactions to the deposition of crystals in the joints. The anti-inflammatory effect of the helium-neon (He-Ne) laser and that of the nonsteroidal anti-inflammatory drugs (NSAIDs) diclofenac, meloxicam, celecoxib, and rofecoxib was studied in acute and chronic arthritis produced by hydroxyapatite and calcium pyrophosphate in rats. The presence of the markers fibrinogen, L-citrulline, nitric oxide, and nitrotyrosine was determined. Crystals were injected into the posterior limb joints of the rats. A dose of 8 J/cm(2) of energy from an He-Ne laser was applied for 3 d in some groups and for 5 d in other groups. The levels of some of the biomarkers were determined by spectrophotometry, and that of nitrotyrosine was determined by ELISA. For statistical analysis, Fishers exact test was used, and p +/- 0.05 was considered significant. In arthritic rats, the fibrinogen, L-citrulline, nitric oxide, and nitrotyrosine levels increased in comparison to controls and to the laser-treated arthritic groups (p +/- 0.001), (p +/- 0.001), (p +/- 0.02), and (p +/- 0.01), respectively. When comparing fibrinogen from arthritic rats with disease induced by hydroxyapatite with undiseased and arthritic rats treated with NSAIDs, the He-Ne laser decreased levels to values similar to those seen in controls (p +/- 0.01). Inflammatory and oxidative stress markers in experimental crystalopathy are positively modified by photobiostimulation.

Simvastatin: pharmacological response in experimental hyperfibrinogenaemias.

Through a disorder in the endothelial haemostatic balance, hyperfibrinogenaemia could generate endothelial dysfunction. Statins would have antiinflammatory effects on injured endothelium. Objective — Simvastatin pharmacological response in rats with hyperfibrinogenaemias induced by laparotomies was studied. Methods and results — Rats were subjected to multiple injuries (MI) for 30 days (1 laparotomy/week) and for 60 days (1 laparotomy/2 weeks). Simvastatin (0.035 mg/kg) was administered orally to the 30-day multiple injuries group after the third injury for a period of 10 days. A similar dose was administered to the 60-day multiple injuries group after the second injury for a period of 45 days. Blood samples of all the groups were obtained 72 hours after the last injury. In the 30 and 60-day multiple injuries groups, a statistically significant fibrinogen increase was observed (336.6 ± 7.5 and 358.7 ± 9.9, respectively) compared with the control group (207.0 ± 3.0) (p < 0.001).There were no significant differences in the plasmatic fibrinogen (PF) levels between the control and simvastatin treated groups (224.9 ± 1.4 and 216.3 ± 4.3, respectively).There were significant differences between the 30 or 60-day MI untreated groups compared with the 30 or 60-day multiple injuries + simvastatin treated group (p < 0.001). Endothelial denudation and intima widening were observed in the untreated injured groups, whereas in the 60 day multiple injuries group + simvastatin, a regression of histopathological lesions was observed. Conclusions — the decrease of the inflammatory component that would accompany early atherogenesis processes and the regression of the histopathological lesions after treatment could be attributed to the decreased plasmatic fibrinogen.