A common oral pathogen Porphyromonas gingivalis induces myocarditis in rats.

AIM: To evaluate whether Porphyromonas gingivalis (P. gingivalis) inoculation could induce cardiac remodelling in rats. MATERIALS AND METHODS: The study was conducted on 33 Wistar rats, which were distributed in the following experimental groups: not inoculated; inoculated with 1 × 108 CFU/ml of bacteria; inoculated with 3 × 108 CFU/ml of bacteria. The animals were inoculated at baseline and on the 15th day of follow-up. Blood collection was performed at baseline and 60 min after each inoculation. At 29 days, the animals were subjected to echocardiography and at 30 days to haemodynamic studies before sacrificing them. RESULTS: Impact of the bacteria was more evident in rats that received higher P. gingivalis concentration. Thus, 3 × 108 CFU/ml of bacteria increased the rectal temperature and water content in the lung as well as myocardial necrosis and fibrosis. P. gingivalis induced the intensification of DNA fragmentation and increased the levels of malondialdehyde, oxidized proteins, and macrophage expression in the myocardium. These findings were associated with lower LV isovolumetric relaxation time, +dP/dt, -dP/dt, and higher end-diastolic pressure. CONCLUSIONS: P. gingivalis bacteraemia is significantly associated with adverse cardiac remodelling and may play a biological role in the genesis of heart failure.

Post-resistance exercise photobiomodulation therapy has a more effective antioxidant effect than pre-application on muscle oxidative stress.

This study evaluated the effect of photobiomodulation therapy (PBMt) before or after a high-intensity resistance exercise (RE) session on muscle oxidative stress. Female Wistar rats were assigned to one of the following groups: Sham (non-exercised, undergoing placebo-PBMt); NLRE (exercised, undergoing placebo-PBMt); PBMt + RE (pre-exercise PBMt); RE + PBMt (post-exercise PBMt). The RE comprised four climbs bearing the maximum load with a 2 min rest between each climb. An 830-nm aluminum gallium arsenide diode laser (100 mW; 0.028 cm2; 3.57 mW/cm2; 142.8 J/cm2; 4 J; Photon Laser III, DMC, São Paulo, Brazil) was applied 60 s before or after RE in gastrocnemius muscles. Analyses were performed at 24 h after RE: lipoperoxidation using malondialdehyde (MDA) and protein oxidation (OP) on Western blot. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activity were spectrophotometrically assessed. Nitric oxide (NO) level was determined by the Griess reaction. The MDA and OP levels were significantly higher in the NLRE group. Increased OP was prevented in all PBMt groups; however, increased MDA was prevented only in the RE + PBMT group. The RE + PBMt group had higher SOD activity compared to all other groups. A higher GPx activity was observed only in the PBMT + RE compared to Sham group, and CAT activity was reduced by RE, without PBMt effect. NO levels were unchanged with RE or PBMt. Therefore, PBMt application after a RE section has a more potent antioxidant effect than previous PBMt. Rats submitted to post-RE PBMt illustrated prevention of increased lipoperoxidation and protein oxidation as well as increased SOD activity. The photobiomodulation can attenuate oxidative stress induced by resistance exercise. A more evident benefit shows to be obtained with the application after exercise, in which it has increased the activity of superoxide dismustase.

Low-level laser therapy prevents muscle oxidative stress in rats subjected to high-intensity resistance exercise in a dose-dependent manner.

High-intensity resistance exercise (RE) increases oxidative stress leading to deleterious effects on muscle performance and recovery. The aim of this study was to assess the effect of applying low-level laser therapy (LLLT) prior to a RE session on muscle oxidative stress and to determine the possible influence of the dosimetric parameters. Female Wistar rats were assigned to non-LLLT (Ctr: non-exercised control; RNI: RE) or LLLT groups subjected to RE (radiant energy: 4 J, 8 J, and 12 J, respectively). RE consisted of four maximum load climbs. An 830-nm DMC Lase Photon III was used to irradiate three points in gastrocnemius muscles (two limbs) before exercise. Animals were euthanized after 60 min after the end of the exercise, and muscle tissue was removed for analysis of oxidative stress markers. All doses resulted in the prevention of increased lipoperoxidation; however, LLLT prevented protein oxidation only in rats that were pretreated with 8 J and 12 J of energy by LLLT. RE and LLLT did not change catalase activity. However, RE resulted in lower superoxide dismutase activity, and the opposite was observed in the LLLT group. These data indicate that LLLT prior to RE can prevent muscle oxidative stress. This study is the first to evaluate the impact of dosimetric LLLT parameters on the oxidative stress induced by RE, wherein both 8 J and 12 J of energy afforded significant protection.

Protective effects of photobiomodulation against resistance exercise-induced muscle damage and inflammation in rats.

We investigated whether low-level laser therapy (LLLT) prior to or post resistance exercise could attenuate muscle damage and inflammation. Female Wistar rats were assigned to non-LLLT or LLLT groups. An 830-nm DMC Laser Photon III was used to irradiate their hind legs with 2J, 4J, and 8J doses. Irradiations were performed prior to or post (4J) resistance exercise bouts. Resistance exercise consisted of four maximum load climbs. The load work during a resistance exercise bout was similar between Control (non-LLLT, 225 ± 10 g), 2J (215 ± 8 g), 4J (210 ± 9 g), and 8J (226 ± 9 g) groups. Prior LLLT did not induce climbing performance improvement, but exposure to 4J irradiation resulted in lower blood lactate levels post-exercise. The 4J dose decreased creatine kinase and lactic dehydrogenase levels post-exercise regardless of the time of application. Moreover, 4-J irradiation exposure significantly attenuated tumor necrosis factor alpha, interleukin-6, interleukin-1ß, cytokine-induced neutrophil chemoattractant-1, and monocyte chemoattractant protein-1. There was minor macrophage muscle infiltration in 4J-exposed rats. These data indicate that LLLT prior to or post resistance exercise can reduce muscle damage and inflammation, resulting in muscle recovery improvement. We attempted to determine an ideal LLLT dose for suitable results, wherein 4J irradiation exposure showed a significant protective role.

Association of Exercise Training with Tobacco Smoking Prevents Fibrosis but has Adverse Impact on Myocardial Mechanics.

INTRODUCTION: There was no data for cardiac repercussion of exercise training associated with tobacco smoking. This issue is interesting because some smoking people can be enrolled in an exercise-training program. Thus, we evaluated swimming training effects on the function and structural myocardial in rats exposed to tobacco smoking. METHODS: Male Wistar rats were assigned to one of four groups: C, untrained rats without exposure to tobacco smoking; E, exercised rats without exposure to tobacco smoking; CS, untrained rats exposed to tobacco smoking; ECS, exercised rats exposed to tobacco smoking. Rats swam five times a week twice daily (60min per session) for 8 weeks. Before each bout exercise, rats breathed smoke from 20 cigarettes for 60min. Twenty-four hours after the last day of the protocol, papillary muscles were isolated for in vitro analysis of myocardial mechanics. The myocardial mass and nuclear cardiomyocyte volume were used as hypertrophy markers, and collagen content was determined by picrosirius red staining. RESULTS: There was a well-pronounced myocardial hypertrophic effect for two interventions. The exercise blunted myocardial collagen increases induced by tobacco smoking. However, exercise and tobacco-smoking association was deleterious to myocardial performance. Thereby, in vitro experiments with papillary muscles contracting in isometric showed impairment myocardial inotropism in exercised rats exposed to tobacco smoking. CONCLUSIONS: This work presents novel findings on the role of exercise training on cardiac remodeling induced by tobacco smoking. Although exercise has mitigated tissue fibrosis, their association with tobacco smoking exacerbated hypertrophy and in vitro myocardial dysfunction. IMPLICATIONS: This is first study to show that the association of an aerobic exercise training with tobacco smoking intensifies the phenotype of pathological cardiac hypertrophy. Therefore, the combination of interventions resulted in exacerbated myocardial hypertrophy and contractility dysfunction. These findings have significant clinical implication because some smoking people can be enrolled in an exercise-training program.

Examining the impact of varying low-level laser dose on cardiac failure.

Low-level laser therapy (LLLT) has been targeted as a promising tool that can mitigate post-infarction cardiac remodeling. However, there is no gold standard energy delivered to the heart and few studies have evaluated the impact of LLLT on cardiac performance. This study evaluated effects of repeated LLLT applications with different energies delivered to the infarcted myocardium. Echocardiography and hemodynamic measurements were applied to evaluate left ventricular (LV) performance in rats with large infarcts. ELISA, Western blot and biochemical assays were used to assess LV inflammation and oxidative stress. An 830-nm Laser Photon III semiconductor aluminum gallium arsenide diode (DMC, São Carlos, SP, Brazil) was applied transthoracically three times a week for 4 weeks based on the energy (i.e., 10J, 20J, and 40J; respectively). LLLT on 10J and 20J had a similar action in attenuating pulmonary congestion and myocardial fibrosis. Moreover, 10J and 20J attenuated LV end-diastolic pressure and improved +dP/dt and -dP/dt. All LLLT groups had lower levels of inflammatory mediators, but only the 10J group had normalized oxidative stress. All LLLT doses improved superoxide dismutase levels; however, only the 20J group showed a high content of the catalase. There was a lower level of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a in the infarcted myocardium, which it was normalized in the 20J and 40J groups. A higher phospholamban content was found in the 10J group. This study supports the beneficial LLLT role post-infarction. Apparently, the 10J and 20J doses show to be chosen for clinical translation.

How long does the biological effect of a red light-emitting diode last on adipose-derived mesenchymal stem cells?

This research investigated the duration of the influence of red light-emitting diodes (LED, 630 nm; output power: 2452.5 mW; laser beam: 163.5 cm2; irradiance: 15 mW/cm2; radiant exposure: 4 J/cm2) on different periods after irradiation (6, 12, 24, 48, and 72 h) on adipose-derived mesenchymal stem cells' (AdMSCs) metabolism and paracrine factors. AdMSCs were irradiated three times every 48 h. Twenty-four hours after the last irradiation, there was a higher MTT absorbance, followed by a decrease after 48 h. The cells' secretome showed increased levels of IL-6 and VEGF after 12 and 24 h, but this was reversed after 48 h. Additionally, LED irradiation resulted in higher levels of nitrite and did not affect oxidative stress markers. LED irradiation had significant effects on AdMSCs after 24 h compared to other groups and its control group.

Light-emitting Diode Can Enhance the Metabolism and Paracrine Action of Mesenchymal Stem Cells.

This study investigated the influence of red light-emitting diodes (LED, 630 nm) on different irradiation parameters and the number of applications on mesenchymal stem cells derived from adipose tissue (AdMSCs) metabolism and paracrine factors. The AdMSCs were irradiated with a LEDbox device (output power: 2452.5 mW; laser beam: 163.5 cm2 ; irradiance: 15 mW cm-2 ) using radiant exposures of 0.5, 2, and 4 J cm-2 , respectively. AdMSCs were irradiated once or every 48 h up to three irradiations. All molecular analyses were performed 24 h after the last irradiation. LED did not induce changes in cell count, DNA damage, and oxidative stress. A significant repercussion of the LED has been noticed after three irradiations with 4 J cm-2 . AdMSCs had higher levels of IL-6, IGF-1, and NOx index. A higher ATP content and MMT/Resazurin assay were identified in AdMSCs irradiated three times with 4 J cm-2 . Mitochondrial basal respiration, maximal respiration and proton leak under metabolic stress were reduced by 0.5 and 2 J cm-2 irradiations. These data showed that three LED irradiations with 4 J cm-2 may be a suitable parameter for future AdMSCs therapy because of its improved metabolic activity, ATP content, and IL-6, IGF-1, and nitric oxide secretion.

Photobiomodulation therapy combined with carvedilol attenuates post-infarction heart failure by suppressing excessive inflammation and oxidative stress in rats.

The post-myocardial infarction heart failure (HF) still carries a huge burden since current therapy is unsuccessful to abrogate poor prognosis. Thus, new approaches are needed, and photobiomodulation therapy (PBMt) may be a way. However, it is not known whether PBMt added to a standard HF therapy provides additional improvement in cardiac remodeling in infarcted rats. This study sought to determine the combined carvedilol-drug and PBMt with low-level laser therapy value in HF. Rats with large infarcts were treated for 30 days. The functional fitness was evaluated using a motorized treadmill. Echocardiography and hemodynamic measurements were used for functional evaluations of left ventricular (LV). ELISA, Western blot and biochemical assays were used to evaluate inflammation and oxidative stress in the myocardium. Carvedilol and PBMt had a similar action in normalizing pulmonary congestion and LV end-diastolic pressure, attenuating LV dilation, and improving LV systolic function. Moreover, the application of PBMt to carvedilol-treated rats inhibited myocardial hypertrophy and improved +dP/dt of LV. PBMt alone prevented inflammation with a superior effect than carvedilol. Carvedilol and PBMt normalized 4-hydroxynonenal (a lipoperoxidation marker) levels in the myocardium. However, importantly, the addition of PBMt to carvedilol attenuated oxidized protein content and triggered a high activity of the anti-oxidant catalase enzyme. In conclusion, these data show that the use of PBMt plus carvedilol therapy results in a significant additional improvement in HF in a rat model of myocardial infarction. These beneficial effects were observed to be due, at least in part, to decreased myocardial inflammation and oxidative stress.

Photobiomodulation Leads to Reduced Oxidative Stress in Rats Submitted to High-Intensity Resistive Exercise.

The aim of this study was to determine whether oxidative stress markers are influenced by low-intensity laser therapy (LLLT) in rats subjected to a high-intensity resistive exercise session (RE). Female Wistar rats divided into three experimental groups (Ctr: control, 4J: LLLT, and RE) and subdivided based on the sampling times (instantly or 24 h postexercise) underwent irradiation with LLLT using three-point transcutaneous method on the hind legs, which was applied to the gastrocnemius muscle at the distal, medial, and proximal points. Laser (4J) or placebo (device off) were carried out 60 sec prior to RE that consisted of four climbs bearing the maximum load with a 2 min time interval between each climb. Lipoperoxidation levels and antioxidant capacity were obtained in muscle. Lipoperoxidation levels were increased (4-HNE and CL markers) instantly post-RE. LLLT prior to RE avoided the increase of the lipid peroxidation levels. Similar results were also notified for oxidation protein assays. The GPx and FRAP activities did not reduce instantly or 24 h after RE. SOD increased 24 h after RE, while CAT activity did not change with RE or LLLT. In conclusion, LLLT prior to RE reduced the oxidative stress markers, as well as, avoided reduction, and still increased the antioxidant capacity.