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IntroductionInflammation of the synovial membrane plays an important role in the pathophysiology of osteoarthritis (OA). The synovial tissue of patients with initial OA is characterized by infiltration of mononuclear cells and production of proinflammatory cytokines and other mediators of joint injury. The objective was to evaluate the effect of low-level laser therapy (LLLT) operating at 50 mW and 100 mW on joint inflammation in rats induced by papain, through histopathological analysis, differential counts of inflammatory cells (macrophages and neutrophils), as well as gene expression of interleukin 1-beta and 6 (IL-1β and IL-6), and protein expression of tumor necrosis factor alpha (TNFα).MethodsMale Wistar rats (n = 60) were randomly divided into four groups of 15 animals, namely: a negative control group; an inflammation injury positive control group; a 50 mW LLLT group, subjected to injury and treated with 50 mW LLLT; and a 100 mW LLLT group, subjected to injury and treated with 100 mW LLLT. The animals were subject to joint inflammation (papain solution, 4%) and then treated with LLLT (808 nm, 4 J, 142.4 J/cm2, spot size 0.028 for both groups). On the day of euthanasia, articular lavage was collected and immediately centrifuged; the supernatant was saved for analysis of expression of TNFα protein by enzyme-linked immunosorbent assay and expression of IL-1β and IL-6 mRNA by real-time polymerase chain reaction. A histologic examination of joint tissue was also performed. For the statistical analysis, analysis of variance with Tukey's post-hoc test was used for comparisons between each group. All data are expressed as mean values and standard deviation, with P < 0.05.ResultsLaser treatment with 50 mW was more efficient than 100 mW in reducing cellular inflammation, and decreased the expression of IL-1β and IL-6. However, the 100 mW treatment led to a higher reduction of TNFα compared with the 50 mW treatment.ConclusionsLLLT with 50 mW was more efficient in modulating inflammatory mediators (IL-1β, IL-6) and inflammatory cells (macrophages and neutrophils), which correlated with the histology that showed a reduction in the inflammatory process.

The aim of the present study was to determine the effect of low-level laser therapy (LLLT) on the expression of TNF-α and TGF-β in the tibialis anterior muscle of rats following cryoinjury. Muscle regeneration involves cell proliferation, migration and differentiation and is regulated by growth factors and cytokines. A growing body of evidence suggests that LLLT promotes skeletal muscle regeneration by reducing the duration of acute inflammation and accelerating tissue repair. Adult male Wistar rats (n = 35) were randomly divided into three groups: control group (no lesion, untreated, n = 5), cryoinjury without LLLT group (n = 15), and cryoinjury with LLLT group (n = 15). The injured region was irradiated three times a week using an AlGaInP laser (660 nm; beam spot 0.04 cm(2), output power 20 mW, power density 500 mW/cm(2), energy density 5 J/cm(2), exposure time 10 s). Muscle remodeling was evaluated at 1, 7 and 14 days (long-term) following injury. The muscles were removed and total RNA was isolated using TRIzol reagent and cDNA synthesis. Real-time polymerase chain reactions were performed using TNF-α and TGF-β primers; GAPDH was used to normalize the data. LLLT caused a decrease in TNF-α mRNA expression at 1 and 7 days following injury and in TGF-β mRNA expression at 7 days following cryoinjury in comparison to the control group. LLLT modulated cytokine expression during short-term muscle remodeling, inducing a decrease in TNF-α and TGF-β.

AimThe aim of this study was to investigate the impact of circuit-based exercise on the body composition in obese older women by focusing on physical exercise and body weight (BW) gain control in older people.MethodsSeventy older women (>60 years old) voluntarily took part in the study. Participants were randomized into six different groups according to body mass index (BMI): appropriate weight (AW) control (AWC) and trained (AWT) groups, overweight (OW) control (OWC) and trained (OWT) groups, and obesity (O) control (OC) and trained (OT) groups. The exercise program consisted of 50 minutes of exercise three times per week for 12 weeks. The exercises were alternated between upper and lower body using rest between sets for 40 seconds with intensity controlled by heart rate (70% of work). The contraction time established was 5 seconds to eccentric and concentric muscular action phase. The following anthropometric parameters were evaluated: height (m), body weight (BW, kg), body fat (BF, %), fat mass (FM, kg), lean mass (LM, kg), and BMI (kg/m2).ResultsThe values (mean ± standard deviation [SD]) of relative changes to BW (−8.0% ± 0.8%), BF (−21.4% ± 2.1%), LM (3.0% ± 0.3%), and FM (−31.2% ± 3.0%) to the OT group were higher (P < 0.05) than in the AWT (BW: −2.0% ± 1.1%; BF: −4.6% ± 1.8%; FM: −7.0% ± 2.8%; LM: 0.2% ± 1.1%) and OWT (BW: −4.5% ± 1.0%; BF: −11.0% ± 2.2%; FM: −16.1% ± 3.2%; LM: −0.2% ± 1.0%) groups; additionally, no differences were found for C groups. While reduction (P < 0.03) in BMI according to absolute values was observed for all trained groups (AWT: 22 ± 1 versus 21 ± 1; OWT: 27 ± 1 versus 25 ± 1, OT: 34 ± 1 versus 30 ± 1) after training, no differences were found for C groups.ConclusionIn summary, circuit-based exercise is an effective method for promoting reduction in anthropometrics parameters in obese older women.

Abstract-The potential involvement of the brain renin-angiotensin system in the hypertension induced by subpressor doses of angiotensin II was tested by the use of newly developed transgenic rats with permanent inhibition of brain angiotensinogen synthesis [TGR(ASrAOGEN)]. Basal systolic blood pressure monitored by telemetry was significantly lower in TGR(ASrAOGEN) than in Sprague-Dawley rats (parent strain) (122.5Ϯ1.5 versus 128.9Ϯ1.9 mm Hg, respectively; PϽ0.05). The increase in systolic blood pressure induced by 7 days of chronic angiotensin II infusion was significantly attenuated in TGR(ASrAOGEN) in comparison with control rats (29.8Ϯ4.2 versus 46.3Ϯ2.5 mm Hg, respectively; PϽ0.005). Moreover, an increase in heart/body weight ratio was evident only in Sprague-Dawley (11.1%) but not in TGR(ASrAOGEN) rats (2.8%). In contrast, mRNA levels of atrial natriuretic peptide (ANP) and collagen III in the left ventricle measured by ribonuclease protection assay were similarly increased in both TGR(ASrAOGEN) (ANP, ϫ2.5; collagen III, ϫ1.8) and Sprague-Dawley rats (ANP, ϫ2.4; collagen III, ϫ2) as a consequence of angiotensin II infusion. Thus, the expression of these genes in the left ventricle seems to be directly stimulated by angiotensin II. However, the hypertensive and hypertrophic effects of subpressor angiotensin II are at least in part mediated by the brain renin-angiotensin system. Key Words: renin-angiotensin system Ⅲ collagen Ⅲ angiotensin II Ⅲ hypertrophy Ⅲ atrial natriuretic peptide T he renin-angiotensin system (RAS) is acknowledged to play an important role in the pathophysiology of hypertension and cardiovascular diseases. Since tissue RASs have been postulated, local formation of angiotensin II (Ang II) is consistently invoked to explain that RAS inhibitors can exert beneficial effects in cardiovascular diseases, even in the absence of Ang II plasma levels that directly increase blood pressure (BP). 1 The mechanisms by which increases in plasma Ang II can induce an increase in BP in these situations are still not clearly defined. One experimental animal model designed to mimic human hypertension that is often used to obtain insights regarding its pathophysiological mechanisms is attained by chronic infusion (days to weeks) of subpressor doses of Ang II. 2 Infused doses of Ang II up to 250 ng/kg per minute SC that do not produce direct vasoconstriction are described as "subpressor" or "slow pressor" and can induce a gradual increase of BP. Several studies have indicated that the central nervous system is involved in the effects of the subpressor Ang II. Arguments are based on the elimination of the hypertensive effect of Ang II by ablation of area postrema 3 or lateral parabrachial nucleus. 4 Furthermore, the hypertensive effect of subpressor doses of Ang II can be inhibited by central sympathoinhibitors, 5 ganglionic blockers, 6 nonselective ␣-blockade, 7 or renal denervation, 8 supporting a neurogenic pressor mechanism.The role of the brain RAS in the central control of cardiovascular homeostasis and p...