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De Lima F.M.,Research and Development Institute IPandD | Moreira L.M.,Praca Dom Helvecio | Villaverde A.B.,Institute of Biomedical Engineering | Albertini R.,Centro Universitario Nove Of Julho Uninove | And 2 more authors.
Lasers in Medical Science | Year: 2011

The aim of this work was to investigate if the low-level laser therapy (LLLT) on acute lung inflammation (ALI) induced by lipopolysaccharide (LPS) is linked to tumor necrosis factor (TNF) in alveolar macrophages (AM) from bronchoalveolar lavage fluid (BALF) of mice. LLLT has been reported to actuate positively for relieving the late and early symptoms of airway and lung inflammation. It is not known if the increased TNF mRNA expression and dysfunction of cAMP generation observed in ALI can be influenced by LLLT. For in vivo studies, Balb/c mice (n=5 for group) received LPS inhalation or TNF intra nasal instillation and 3 h after LPS or TNF-α, leukocytes in BALF were analyzed. LLLT administered perpendicularly to a point in the middle of the dissected bronchi with a wavelength of 660 nm and a dose of 4.5 J/cm 2. The mice were irradiated 15 min after ALI induction. In vitro AM from mice were cultured for analyses of TNF mRNA expression and protein and adenosine3':5'-cyclic monophosphate (cAMP) levels. One hour after LPS, the TNF and cAMP levels in AM were measured by ELISA. RT-PCR was used to measure TNF mRNA in AM. The LLLT was inefficient in potentiating the rolipram effect in presence of a TNF synthesis inhibitor. LLLT attenuated the neutrophil influx and TNF in BALF. In AM, the laser increased the cAMP and reduced the TNF-α mRNA. LLLT increases indirectly the cAMP in AM by a TNF-dependent mechanism. © 2010 Springer-Verlag London Ltd. Source

Silva V.R.,Nove de Julho University | Marcondes P.,Federal University of Sao Paulo | Silva M.,Nove de Julho University | Villaverde A.B.,Institute of Biomedical Engineering | And 4 more authors.
Respiratory Physiology and Neurobiology | Year: 2014

Low-level laser therapy (LLLT) controls bronchial hyperresponsiveness (BHR) associated with increased RhoA expression as well as pro-inflammatory mediators associated with NF-kB in acute lung inflammation. Herein, we explore if LLLT can reduce both BHR and Th2 cytokines in allergic asthma. Mice were studied for bronchial reactivity and lung inflammation after antigen challenge. BHR was measured through dose-response curves to acetylcholine. Some animals were pretreated with a RhoA inhibitor before the antigen. LLLT (660. nm, 30. mW and 5.4. J) was applied on the skin over the right upper bronchus and two irradiation protocols were used. Reduction of BHR post LLLT coincided with lower RhoA expression in bronchial muscle as well as reduction in eosinophils and eotaxin. LLLT also diminished ICAM expression and Th2 cytokines as well as signal transducer and activator of transduction 6 (STAT6) levels in lungs from challenged mice. Our results demonstrated that LLLT reduced BHR via RhoA and lessened allergic lung inflammation via STAT6. © 2014 Elsevier B.V. Source

De Lima F.M.,Institute of Research and Development | Villaverde A.B.,University Camilo Castelo Branco | Albertini R.,Centro Universitario Nove Of Julho | De Oliveira A.P.L.,Institute of Biomedical science | And 2 more authors.
Photomedicine and Laser Surgery | Year: 2010

Objective: The aim of this work was to investigate the low-level laser therapy (LLLT) effect on alveolar macrophages (AM) activated by oxidative stress and lipopolysaccharide (LPS). Background data: LLLT has been reported to actuate positively relieving the late and early symptoms of airway and lung inflammation. It is not known if the increased MIP-2mRNA expression and intracellular reactive oxygen species (ROS) generation observed in acute lung inflammation (ALI) can be influenced by LLLT. Materials and Methods: Rat AM cell line (AMJ2-C11) was cultured with LPS or H2O2 and laser irradiated. MIP-2mRNA and ROS production in the AM were evaluated by Real Time-PCR and the 2′,7′-dichlorofluorescin diacetate (DCFH-DA) respectively. The NF-κB protein in the AM was measured by the enzyme linked immunoassay method. To investigate the antioxidant effect of laser, the AM were prebathed with N-acetylcysteine (NAC) and then irradiated with laser. LLLT was also studied in the presence of an inhibitor of NF-κB (BMS 205820). In addition, the effect of LLLT on NF-κB protein was investigated. Results: LLLT attenuated the MIP-2mRNA expression and intracellular ROS generation after LPS or H2O2. When the AM were pretreated with NAC, the laser effect was potentiated. BMS 205820 suppresses the effect of LLLT on MIP-2mRNA expression and ROS generation, stimulated by LPS or H2O2. On NF-κB transcription factor, both the LLLT and NAC reduced this protein in the AM exposed to LPS or H2O2. The synergistic effect between LLLT and NAC on the reduction the NF-κB was also evidenced. Conclusion: Results indicate that there is a synergistic action of LLLT with NAC on MIP-2mRNA expression from LPS- or H2O2-stimulated AM, and that both ROS intracellular generation and NF-kB signaling seem to be involved. Copyright 2010, Mary Ann Liebert, Inc. Source

De Lima F.M.,Nove de Julho University | Albertini R.,Nove de Julho University | Dantas Y.,Intesive Care Unity | Maia-Filho A.L.,Faculty Integral Diferencial FACID | And 5 more authors.
Photochemistry and Photobiology | Year: 2013

It remains unknown if the oxidative stress can be regulated by low-level laser therapy (LLLT) in lung inflammation induced by intestinal reperfusion (i-I/R). A study was developed in which rats were irradiated (660 nm, 30 mW, 5.4 J) on the skin over the bronchus and euthanized 2 h after the initial of intestinal reperfusion. Lung edema and bronchoalveolar lavage fluid neutrophils were measured by the Evans blue extravasation and myeloperoxidase (MPO) activity respectively. Lung histology was used for analyzing the injury score. Reactive oxygen species (ROS) was measured by fluorescence. Both expression intercellular adhesion molecule 1 (ICAM-1) and peroxisome proliferator-activated receptor-y (PPARy) were measured by RT-PCR. The lung immunohistochemical localization of ICAM-1 was visualized as a brown stain. Both lung HSP70 and glutathione protein were evaluated by ELISA. LLLT reduced neatly the edema, neutrophils influx, MPO activity and ICAM-1 mRNA expression. LLLT also reduced the ROS formation and oppositely increased GSH concentration in lung from i-I/R groups. Both HSP70 and PPARy expression also were elevated after laser irradiation. Results indicate that laser effect in attenuating the acute lung inflammation is driven to restore the balance between the pro- and antioxidants mediators rising of PPARy expression and consequently the HSP70 production. This diagram shows the mechanism of action by which low-level laser therapy controls the acute lung inflammation and restores the oxidative-stress balance in experimental model of trauma induced by intestinal ischemia and reperfusion. © 2012 Wiley Periodicals, Inc. Photochemistry and Photobiology © 2012 The American Society of Photobiology. Source

Paiva L.A.,Laboratory of Immunopharmacology | Coelho K.A.,Laboratory of Immunopharmacology | Luna-Gomes T.,Federal University of Rio de Janeiro | El-Cheikh M.C.,Federal University of Rio de Janeiro | And 4 more authors.
Prostaglandins Leukotrienes and Essential Fatty Acids | Year: 2015

Hepatic Stellate Cells (HSCs) play a crucial role in pathogenesis of liver inflammation and fibrosis. During chronic liver injury, HSCs lose vitamin A and transform into myofibroblastic cells. In schistosomal granulomas, these activated HSCs are called GR-HSCs. Schistosomal-triggered hepatic fibrogenesis has TGF-β as the most potent fibrogenic stimulus, that also controls gene expression of the angiogenic molecule VEGF in HSCs. COX-dependent production of prostaglandins (PGs) also play role in angiogenic processes. Besides angiogenic roles, prostanoids control immunomodulation of Schistosoma mansoni infection. Specifically, schistosoma-derived PGD2 has emerged as a key parasite regulator of immune defense evasion, while no role is still established to host PGD2. Therefore, the aim of this work is to investigate the ability of GR-HSCs to synthesize COX-derived PGD2 and a potential role of this prostanoid in VEGF production by GR-HSCs in vitro. Here, we confirmed that GR-HSCs express COX-2, which displayed perinuclear localization. While unstimulated GR-HSCs produce basal levels of PGD2, TGF-β stimulation besides increasing COX2- mRNA levels, enhanced synthesis/secretion of PGD2 in GR-HSCs supernatant. Moreover, GR-HSCs-derived PGD2 mediate VEGF production by TGF-β-stimulated GR-HSCs, since the pre-treatment with HQL-79, an inhibitor of hematopoietic PGD synthase inhibited both PGD2 synthesis and VEGF secretion by TGF-β-stimulated GR-HSCs. All together, our findings show an autocrine/paracrine activity of GR-HSCs-derived PGD2 on TGF-β-induced VEGF production by GR-HSCs, unveiling a role for PGD2 as important regulator of HSCs activation in hepatic granulomas from schistosome infected mice. © 2015 Elsevier Ltd. Source

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