RESUMO

The objective of this research was to evaluate the interference of ethanol consumption by female rats with cytokines involved in the sepsis process and its correlation with mortality, the main outcome of sepsis. Female Wistar rats in estrus phase were evaluated in three experiments. Experiment 1 (n=40) was performed to determine survival rates. Experiment 2 (n=69) was designed for biochemical analysis, measurement of cytokine and estrogen levels before and after sepsis, and experiment 3 (n=10) was performed to evaluate bacterial growth by colony counts of peritoneal fluid. In all experiments, treated animals were exposed to a 10% ethanol/water solution (v/v) as the single drinking source, while untreated animals were given tap water. After 4 weeks, sepsis was induced in the rats by ip injection of feces. In experiment 1, mortality in ethanol-exposed animals was delayed compared with those that drank water (48 h; P=0.0001). Experiment 2 showed increased tumor necrosis factor alpha (TNF-α) and decreased interleukin-6 (IL-6) and macrophage migration inhibitory factor in septic animals exposed to ethanol compared to septic animals not exposed. Sepsis also increased TNF-α and IL-6 levels in both ethanol- and water-exposed groups. Biochemical analysis showed higher creatinine, alanine aminotransferase and aspartate aminotransferase and decreased glucose levels in septic animals that were exposed to ethanol. In experiment 3, septic animals exposed to ethanol showed decreased numbers of colony-forming units than septic animals exposed to water. These results suggest that ethanol consumption delays the mortality of female rats in estrus phase after sepsis induction. Female characteristics, most probably sex hormones, may be involved in cytokine expression.

RESUMO

The objective of this research was to evaluate the interference of ethanol consumption by female rats with cytokines involved in the sepsis process and its correlation with mortality, the main outcome of sepsis. Female Wistar rats in estrus phase were evaluated in three experiments. Experiment 1 (n=40) was performed to determine survival rates. Experiment 2 (n=69) was designed for biochemical analysis, measurement of cytokine and estrogen levels before and after sepsis, and experiment 3 (n=10) was performed to evaluate bacterial growth by colony counts of peritoneal fluid. In all experiments, treated animals were exposed to a 10% ethanol/water solution (v/v) as the single drinking source, while untreated animals were given tap water. After 4 weeks, sepsis was induced in the rats by ip injection of feces. In experiment 1, mortality in ethanol-exposed animals was delayed compared with those that drank water (48 h; P=0.0001). Experiment 2 showed increased tumor necrosis factor alpha (TNF-α) and decreased interleukin-6 (IL-6) and macrophage migration inhibitory factor in septic animals exposed to ethanol compared to septic animals not exposed. Sepsis also increased TNF-α and IL-6 levels in both ethanol- and water-exposed groups. Biochemical analysis showed higher creatinine, alanine aminotransferase and aspartate aminotransferase and decreased glucose levels in septic animals that were exposed to ethanol. In experiment 3, septic animals exposed to ethanol showed decreased numbers of colony-forming units than septic animals exposed to water. These results suggest that ethanol consumption delays the mortality of female rats in estrus phase after sepsis induction. Female characteristics, most probably sex hormones, may be involved in cytokine expression.

RESUMO

Leptospirosis is an important zoonosis and has a worldwide impact on public health. This paper will discuss both the role of immunogenic and pathogenic molecules during leptospirosis infection and possible new targets for immunotherapy against leptospira components. Leptospira, possess a wide variety of mechanisms that allow them to evade the host immune system and cause infection. Many molecules contribute to the ability of Leptospira to adhere, invade, and colonize. The recent sequencing of the Leptospira genome has increased our knowledge about this pathogen. Although the virulence factors, molecular targets, mechanisms of inflammation, and signaling pathways triggered by leptospiral antigens have been studied, some questions are still unanswered. Toll-like receptors (TLRs) are the primary sensors of invading pathogens. TLRs recognize conserved microbial pattern molecules and activate signaling pathways that are pivotal to innate and adaptive immune responses. Recently, a new molecular target has emerged--the Na/K-ATPase--which may contribute to inflammatory and metabolic alteration in this syndrome. Na/K-ATPase is a target for specific fatty acids of host origin and for bacterial components such as the glycolipoprotein fraction (GLP) that may lead to inflammasome activation. We propose that in addition to TLRs, Na/K-ATPase may play a role in the innate response to leptospirosis infection.

Assuntos

Inflamação/imunologia , Inflamação/metabolismo , Leptospirose/imunologia , Leptospirose/metabolismo , Animais , Humanos , Transdução de Sinais/fisiologia , ATPase Trocadora de Sódio-Potássio/metabolismo , Receptores Toll-Like/metabolismo

RESUMO

Sepsis is a severe disorder characterized by systemic inflammatory responses in the presence of an infection and may progress to multiple organ dysfunction and death. Alterations in cerebral microcirculation fulfill a crucial role in the pathogenesis of severe sepsis, and include a decrease in capillary density and disturbances in leukocyte movement along capillaries. Nevertheless, the mechanisms involved in sepsis-associated cerebral microcirculatory alterations have so far not been defined. We investigated the effect of the peroxisome proliferator-activated receptor gamma (PPARγ) selective agonist rosiglitazone on leukocyte/endothelial cell interaction and functional capillary density in the brain in the cecal ligation and puncture (CLP) model of sepsis. Anti-inflammatory effects of rosiglitazone on the cerebral microcirculation were marked. Functional capillary density increased and leukocyte rolling and adhesion were decreased in animals submitted to CLP and treated with rosiglitazone. Our data provide evidence for involvement of PPARγ activation in leukocyte-endothelium interactions and alterations in capillary density. Improved cerebral perfusion in animals treated with rosiglitazone, suggests that PPARγ activation is protective against cerebral microvascular dysfunction in sepsis.

Assuntos

Anti-Inflamatórios/farmacologia , Encéfalo/irrigação sanguínea , Circulação Cerebrovascular/efeitos dos fármacos , Transtornos Cerebrovasculares/prevenção & controle , Microcirculação/efeitos dos fármacos , Microvasos/efeitos dos fármacos , PPAR gama/agonistas , Sepse/tratamento farmacológico , Tiazolidinedionas/farmacologia , Animais , Ceco/cirurgia , Transtornos Cerebrovasculares/imunologia , Transtornos Cerebrovasculares/metabolismo , Transtornos Cerebrovasculares/fisiopatologia , Citoproteção , Modelos Animais de Doenças , Migração e Rolagem de Leucócitos/efeitos dos fármacos , Ligadura , Masculino , Camundongos , Microvasos/imunologia , Microvasos/metabolismo , Microvasos/fisiopatologia , Infiltração de Neutrófilos/efeitos dos fármacos , PPAR gama/metabolismo , Punções , Rosiglitazona , Sepse/imunologia , Sepse/metabolismo , Sepse/fisiopatologia

RESUMO

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-2 mRNA 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 H(2)O(2) and laser irradiated. MIP-2 mRNA 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-2 mRNA expression and intracellular ROS generation after LPS or H(2)O(2). When the AM were pretreated with NAC, the laser effect was potentiated. BMS 205820 suppresses the effect of LLLT on MIP-2 mRNA expression and ROS generation, stimulated by LPS or H(2)O(2). On NF-κB transcription factor, both the LLLT and NAC reduced this protein in the AM exposed to LPS or H(2)O(2). 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-2 mRNA expression from LPS- or H(2)O(2)-stimulated AM, and that both ROS intracellular generation and NF-kB signaling seem to be involved.

Assuntos

Quimiocina CXCL2/genética , Terapia com Luz de Baixa Intensidade , Macrófagos Alveolares/metabolismo , RNA Mensageiro/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Acetilcisteína/farmacologia , Animais , Células Cultivadas , Quimiocina CXCL2/metabolismo , Sequestradores de Radicais Livres/farmacologia , Macrófagos Alveolares/efeitos da radiação , Ratos

RESUMO

It has been suggested that low intensity laser therapy (LILT) acts on pulmonary inflammation. Thus, we investigate in this work if LILT (650nm, 2.5mW, 31.2mW/cm(2), 1.3J/cm(2), laser spot size of 0.08cm(2) and irradiation time of 42s) can attenuate edema, neutrophil recruitment and inflammatory mediators in acute lung inflammation. Thirty-five male Wistar rats (n=7 per group) were distributed in the following experimental groups: control, laser, LPS, LPS+laser and dexamethasone+LPS. Airway inflammation was measured 4h post-LPS challenge. Pulmonary microvascular leakage was used for measuring pulmonary edema. Bronchoalveolar lavage fluid (BALF) cellularity and myeloperoxidase (MPO) were used for measuring neutrophil recruitment and activation. RT-PCR was performed in lung tissue to assess mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin (IL-10), cytokine-induced neutrophil chemoattractant-1 (CINC-1), macrophage inflammatory protein-2 (MIP-2) and intercellular adhesion molecule-1 (ICAM-1). Protein levels in both BALF and lung were determined by ELISA. LILT inhibited pulmonary edema and endothelial cytoskeleton damage, as well as neutrophil influx and activation. Similarly, the LILT reduced the TNF-α and IL-1ß, in lung and BALF. LILT prevented lung ICAM-1 up-regulation. The rise of CINC-1 and MIP-2 protein levels in both lung and BALF, and the lung mRNA expressions for IL-10, were unaffected. Data suggest that the LILT effect is due to the inhibition of ICAM-1 via the inhibition of TNF-α and IL-1ß.

Assuntos

Quimiocinas/metabolismo , Citocinas/metabolismo , Terapia com Luz de Baixa Intensidade , Neutrófilos/efeitos da radiação , Pneumonia/radioterapia , Doença Aguda , Aerossóis/química , Animais , Anti-Inflamatórios/farmacologia , Líquido da Lavagem Broncoalveolar , Quimiocina CXCL1/genética , Quimiocina CXCL1/metabolismo , Quimiocina CXCL2/genética , Quimiocina CXCL2/metabolismo , Quimiocinas/genética , Citocinas/genética , Dexametasona/farmacologia , Modelos Animais de Doenças , Escherichia coli/metabolismo , Molécula 1 de Adesão Intercelular/genética , Molécula 1 de Adesão Intercelular/metabolismo , Interleucina-10/genética , Interleucina-10/metabolismo , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Lipopolissacarídeos/toxicidade , Pulmão/imunologia , Pulmão/metabolismo , Pulmão/patologia , Masculino , Neutrófilos/metabolismo , Peroxidase/metabolismo , Ratos , Ratos Wistar , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo

RESUMO

After myocardial infarction (MI), activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). The interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression by analyzing hybridization to AECOM 32k mouse microarrays. Ischemic HF significantly increased the levels of total serum IgM (by 5.2-fold) and total IgG (by 3.6-fold) associated with a relatively high content of anti-heart specificity. A comparable increase was observed in the levels of circulating pro-inflammatory cytokines such as IL-1â (3.8X) and TNF-á (6.0X). IFN-ã was also increased by 3.1-fold in the MI group. However, IL-4 and IL-10 were not significantly different between the MI and sham-operated groups. Chemokines such as MCP-1 and IL-8 were 1.4- and 13-fold increased, respectively, in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by post-ischemic HF. Complement activation and immune response were among the most up-regulated processes. Interestingly, 21 of the 101 quantified unigenes involved in the inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune-mediated mechanisms that act both systemically and locally.

Assuntos

Animais , Feminino , Masculino , Camundongos , Citocinas/sangue , Insuficiência Cardíaca/imunologia , Autoanticorpos/sangue , Modelos Animais de Doenças , Ecocardiografia , Perfilação da Expressão Gênica , Insuficiência Cardíaca/sangue , Insuficiência Cardíaca/etiologia , Imunoglobulina G/sangue , Imunoglobulina M/sangue , Isquemia Miocárdica/complicações , Isquemia Miocárdica/imunologia , Reação em Cadeia da Polimerase Via Transcriptase Reversa

RESUMO

After myocardial infarction (MI), activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). The interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression by analyzing hybridization to AECOM 32k mouse microarrays. Ischemic HF significantly increased the levels of total serum IgM (by 5.2-fold) and total IgG (by 3.6-fold) associated with a relatively high content of anti-heart specificity. A comparable increase was observed in the levels of circulating pro-inflammatory cytokines such as IL-1beta (3.8X) and TNF-alpha (6.0X). IFN-gamma was also increased by 3.1-fold in the MI group. However, IL-4 and IL-10 were not significantly different between the MI and sham-operated groups. Chemokines such as MCP-1 and IL-8 were 1.4- and 13-fold increased, respectively, in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by post-ischemic HF. Complement activation and immune response were among the most up-regulated processes. Interestingly, 21 of the 101 quantified unigenes involved in the inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune-mediated mechanisms that act both systemically and locally.

Assuntos

Citocinas/sangue , Insuficiência Cardíaca/imunologia , Animais , Autoanticorpos/sangue , Modelos Animais de Doenças , Ecocardiografia , Feminino , Perfilação da Expressão Gênica , Insuficiência Cardíaca/sangue , Insuficiência Cardíaca/etiologia , Imunoglobulina G/sangue , Imunoglobulina M/sangue , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Isquemia Miocárdica/complicações , Isquemia Miocárdica/imunologia , Reação em Cadeia da Polimerase Via Transcriptase Reversa

RESUMO

BACKGROUND AND OBJECTIVE: Low-level laser therapy (LLLT) is a known modulator of inflammatory process. Herein we studied the effect of 660 nm diode laser on mRNA levels of neutrophils anti-apoptotic factors in lipopolysaccharide (LPS)-induced lung inflammation. STUDY DESIGN/METHODOLOGY: Mice were divided into 8 groups (n=7 for each group) and irradiated with energy dosage of 7.5 J/cm(2). The Bcl-xL and A1 mRNA levels in neutrophils were evaluated by Real Time-PCR (RT-PCR). The animals were irradiated after exposure time of LPS. RESULTS: LLLT and an inhibitor of NF-kappaB nuclear translocation (BMS 205820) attenuated the mRNA levels of Bcl-xL and A1 mRNA in lung neutrophils obtained from mice subjected to LPS-induced inflammation. CONCLUSION: LLLT reduced the levels of anti-apoptotic factors in LPS inflamed mice lung neutrophils by an action mechanism in which the NF-kappaB seems to be involved.

Assuntos

Terapia com Luz de Baixa Intensidade , Pulmão/imunologia , Pulmão/efeitos da radiação , NF-kappa B/metabolismo , Neutrófilos/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Proteína bcl-X/metabolismo , Animais , Inflamação , Lipopolissacarídeos/imunologia , Masculino , Camundongos , Antígenos de Histocompatibilidade Menor , Neutrófilos/efeitos da radiação , Peptídeos/farmacologia , RNA Mensageiro/metabolismo , RNA Mensageiro/efeitos da radiação

RESUMO

OBJECTIVE: The aim of this study was to investigate if low-level laser therapy (LLLT) can modulate formation of hemorrhagic lesions induced by immune complex. BACKGROUND DATA: There is a lack of information on LLLT effects in hemorrhagic injuries of high perfusion organs, and the relative efficacy of LLLT compared to anti-inflammatory drugs. METHODS: A controlled animal study was undertaken with 49 male Wistar rats randomly divided into seven groups. Bovine serum albumin (BSA) i.v. was injected through the trachea to induce an immune complex lung injury. The study compared the effect of irradiation by a 650-nm Ga-Al-As laser with LLLT doses of 2.6 Joules/cm(2) to celecoxib, dexamethasone, and control groups for hemorrhagic index (HI) and myeloperoxide activity (MPO) at 24 h after injury. RESULTS: The HI for the control group was 4.0 (95% CI, 3.7-4.3). Celecoxib, LLLT, and dexamethasone all induced significantly (p < 0.01) lower HI than control animals at 2.5 (95% CI, 1.9-3.1), 1.8 (95% CI, 1.2-2.4), and 1.5 (95% CI, 0.9-2.1), respectively, for all comparisons to control. Dexamethasone, but not celecoxib, induced a slightly, but significantly lower HI than LLLT (p = 0.04). MPO activity was significantly decreased in groups receiving celecoxib at 0.87 (95% CI, 0.63-1.11), dexamethasone at 0.50 (95% CI, 0.24-0.76), and LLLT at 0.7 (95% CI, 0.44-0.96) when compared to the control group, at 1.6 (95% CI, 1.34-1.96; p < 0.01), but there were no significant differences between any of the active treatments. CONCLUSION: LLLT at a dose of 2.6 Joules/cm(2) induces a reduction of HI levels and MPO activity in hemorrhagic injury that is not significantly different from celecoxib. Dexamethasone is slightly more effective than LLLT in reducing HI, but not MPO activity.

Assuntos

Hemorragia/radioterapia , Doenças do Complexo Imune/complicações , Terapia com Luz de Baixa Intensidade , Pneumopatias/radioterapia , Animais , Anti-Inflamatórios/farmacologia , Celecoxib , Dexametasona/farmacologia , Hemorragia/tratamento farmacológico , Hemorragia/etiologia , Pneumopatias/tratamento farmacológico , Pneumopatias/etiologia , Masculino , Pirazóis/farmacologia , Ratos , Ratos Wistar , Sulfonamidas/farmacologia

RESUMO

Our objective was to investigate if low-level laser therapy (LLLT) could improve respiratory function and inhibit tumor necrosis factor (TNF-alpha) release into the diaphragm muscle of rats after an intravenous injection of lipopolysaccharide (LPS) (5 mg/kg). We randomly divided Wistar rats in a control group without LPS injection, and LPS groups receiving either (a) no therapy, (b) four sessions in 24 h with diode Ga-AsI-Al laser of 650 nm and a total dose of 5.2 J/cm2, or (c) an intravenous injection (1.25 mg/kg) of the TNF-alpha inhibitor chlorpromazine (CPZ). LPS injection reduced maximal force by electrical stimulation of diaphragm muscle from 24.15+/-0.87 N in controls, but the addition of LLLT partly inhibited this reduction (LPS only: 15.01+/-1.1 N vs LPS+LLLT: 18.84+/-0.73 N, P<0.05). In addition, this dose of LLLT and CPZ significantly (P<0.05 and P<0.01, respectively) reduced TNF-alpha concentrations in diaphragm muscle when compared to the untreated control group.

Assuntos

Diafragma/química , Lipopolissacarídeos , Terapia com Luz de Baixa Intensidade , Insuficiência Respiratória/induzido quimicamente , Insuficiência Respiratória/terapia , Fator de Necrose Tumoral alfa/análise , Animais , Clorpromazina/farmacologia , Diafragma/efeitos dos fármacos , Masculino , Distribuição Aleatória , Ratos , Ratos Wistar , Fator de Necrose Tumoral alfa/antagonistas & inibidores

RESUMO

BACKGROUND AND OBJECTIVE: It is unknown if the decreased ability to relax airway smooth muscles in asthma and other inflammatory airways disorders can be influenced by low level laser therapy (LLLT) irradiation. To investigate if LLLT could reduce impairment in inflamed trachea smooth muscles (TSM) in rats. STUDY DESIGN/MATERIALS AND METHODS: Controlled rat study where trachea was dissected and mounted in an organ bath apparatus with or without a TNF-alpha solution. RESULTS: Low level laser therapy administered perpendicularly to a point in the middle of the dissected trachea with a wavelength of 655 nm and a dose of 2.6 J/cm(2), partially restored TSM relaxation response to isoproterenol. Tension reduction was 47.0 % (+/-2.85) in the laser-irradiated group compared to 22.0% (+/-2.21) in the control group (P < 0.01). Accumulation of cAMP was almost normalized after LLLT at 22.3 pmol/mg (+/-2.1) compared to 17.6 pmol/mg (+/-2.1) in the non-irradiated control group (P < 0.01). CONCLUSION: Low level laser therapy partially restores the normal relaxation response in inflamed TSM and normalizes accumulation of cAMP in the presence of isoproterenol.

Assuntos

Terapia com Luz de Baixa Intensidade/métodos , Relaxamento Muscular/efeitos da radiação , Músculo Liso/efeitos da radiação , Traqueia/efeitos da radiação , Fator de Necrose Tumoral alfa/farmacologia , Animais , Técnicas In Vitro , Masculino , Ratos , Ratos Wistar

RESUMO

OBJECTIVE: The aim of this study was to investigate if low-level laser therapy (LLLT) can modulate acute inflammation and tumor necrosis factor (TNFalpha) levels. BACKGROUND DATA: Drug therapy with TNFalpha-inhibitors has become standard treatment for rheumatoid arthritis, but it is unknown if LLLT can reduce or modulate TNFalpha levels in inflammatory disorders. METHODS: Two controlled animal studies were undertaken, with 35 male Wistar rats randomly divided into five groups each. Rabbit antiserum to ovalbumin was instilled intrabronchially in one of the lobes, followed by the intravenous injection of 10 mg of ovalbumin in 0.5 mL to induce acute lung injury. The first study served to define the time profile of TNFalpha activity for the first 4 h, while the second study compared three different LLLT doses to a control group and a chlorpromazine group at a timepoint where TNFalpha activity was increased. The rats in LLLT groups were irradiated within 5 min at the site of injury by a 650-nm Ga-Al-As laser. RESULTS: There was a time-lag before TNFalpha activity increased after BSA injection. TNFalpha levels increased from < or =6.9 (95% confidence interval [CI], 5.6-8.2) units/mL in the first 3 h to 62.1 (95% CI, 60.8-63.4) units/mL (p < 0.001) at 4 h. An LLLT dose of 0.11 Joules administered with a power density of 31.3 mW/cm(2) in 42 sec significantly reduced TNFalpha level to 50.2 (95% CI, 49.4-51.0), p < 0.01 units/mL versus control. Chlorpromazine reduced TNFalpha level to 45.3 (95% CI, 44.0-46.6) units/mL, p < 0.001 versus control. CONCLUSION: LLLT can reduce TNFalpha expression after acute immunocomplex lung injury in rats, but LLLT dose appears to be critical for reducing TNFalpha release.

Assuntos

Líquido da Lavagem Broncoalveolar/química , Inflamação/metabolismo , Terapia com Luz de Baixa Intensidade , Fator de Necrose Tumoral alfa/análise , Animais , Pulmão/metabolismo , Masculino , Modelos Animais , Dosagem Radioterapêutica , Ratos , Ratos Wistar , Traumatismo por Reperfusão/metabolismo

RESUMO

The purpose of this study was to investigate the effect of low level laser therapy (LLLT) on male Wistar rat trachea hyperreactivity (RTHR), bronchoalveolar lavage (BAL) and lung neutrophils influx after Gram-negative bacterial lipopolyssacharide (LPS) intravenous injection. The RTHR, BAL and lung neutrophils influx were measured over different intervals of time (90 min, 6 h, 24 h and 48 h). The energy density (ED) that produced an anti-inflammatory effect was 2.5 J/cm(2), reducing the maximal contractile response and the sensibility of trachea rings to methacholine after LPS. The same ED produced an anti-inflammatory effect on BAL and lung neutrophils influx. The Celecoxib COX-2 inhibitor reduced RTHR and the number of cells in BAL and lung neutrophils influx of rats treated with LPS. Celecoxib and LLLT reduced the PGE(2) and TXA(2) levels in the BAL of LPS-treated rats. Our results demonstrate that LLLT produced anti-inflammatory effects on RTHR, BAL and lung neutrophils influx in association with inhibition of COX-2-derived metabolites.

Assuntos

Hiper-Reatividade Brônquica/radioterapia , Terapia com Luz de Baixa Intensidade/métodos , Pneumonia/radioterapia , Pirazóis/farmacologia , Sulfonamidas/farmacologia , Animais , Líquido da Lavagem Broncoalveolar/citologia , Celecoxib , Quimiotaxia de Leucócito , Dinoprostona/metabolismo , Modelos Animais de Doenças , Mediadores da Inflamação/análise , Lipopolissacarídeos , Masculino , Neutrófilos/citologia , Probabilidade , Distribuição Aleatória , Ratos , Valores de Referência , Sensibilidade e Especificidade , Traqueia/fisiopatologia

RESUMO

Nidularium procerum, a common plant of the Brazilian flora, has not yet been studied for its pharmacological properties. We report here that extracts of N. procerum show both analgesic and anti-inflammatory properties. Oral (p.o.) or intraperitoneal (i.p.) administration of an aqueous crude extract from leaves of N. procerum (LAE) inhibited the writhing reaction induced by acetic acid (ED50 value = 0.2 mg/kg body weight, i.p.) in a dose-dependent manner. This analgesic property was confirmed in rats using two different models of bradykinin-induced hyperalgesia; there was 75% inhibition of pain in the modified Hargreaves assay, and 100% inhibition in the classical Hargreaves assay. This potent analgesic effect was not blocked by naloxone, nor was it observed in the hot plate model, indicating that the analgesic effect is not associated with the activation of opioid receptors in the central nervous system. By contrast, we found that LAE (0.02 microg/ml) selectively inhibited prostaglandin E2 production by cyclooxygenase (COX)-2, but not COX-1, which is a plausible mechanism for the analgesic effect. A crude methanol extract from the leaves also showed similar analgesic activity. An identical extract from the roots of N. procerum did not, however, block acetic acid-induced writhes, indicating that the analgesic compounds are concentrated in the leaves. Finally, we found that LAE inhibited an inflammatory reaction induced by lipopolysaccharide in the pleural cavity of mice.

Assuntos

Analgésicos/farmacologia , Anti-Inflamatórios não Esteroides/farmacologia , Bromeliaceae , Dor/prevenção & controle , Fitoterapia , Extratos Vegetais/farmacologia , Ácido Acético , Administração Oral , Analgésicos/administração & dosagem , Analgésicos/uso terapêutico , Animais , Anti-Inflamatórios não Esteroides/administração & dosagem , Anti-Inflamatórios não Esteroides/uso terapêutico , Bradicinina , Brasil , Relação Dose-Resposta a Droga , Edema/induzido quimicamente , Edema/prevenção & controle , Temperatura Alta , Injeções Intraperitoneais , Lipopolissacarídeos , Masculino , Dor/induzido quimicamente , Extratos Vegetais/administração & dosagem , Extratos Vegetais/uso terapêutico , Folhas de Planta , Raízes de Plantas , Pleurisia/induzido quimicamente , Pleurisia/prevenção & controle , Ratos , Ratos Wistar , Árvores

RESUMO

The purpose of the present study was to investigate the effect of the low power laser therapy on the acute inflammatory process. Male Wistar rats were used. The rat paw oedema was induced by sub-plantar injection of carrageenan, the paw volume was measured before and 1, 2, 3 and 4 h after the injection using a hydroplethysmometer. To investigate the mechanism action of the Ga-Al-As laser on inflammatory oedema, parallel studies were performed using adrenallectomized rats or rats treated with sodium diclofenac. Different laser irradiation protocols were employed for specific energy densities (EDs), exposure times and repetition rates. The rats were irradiated with the Ga-Al-As laser during 80 s each hour. The ED that produced an anti-inflammatory effect were 1 and 2.5 J/cm(2), reducing the oedema by 27% (P<0.05) and 45.4% (P<0.01), respectively. The ED of 2.5 J/cm(2) produced anti-inflammatory effects similar to those produced by the cyclooxigenase inhibitor sodium diclofenac at a dose of 1 mg/kg. In adrenalectomized animals, the laser irradiation failed to inhibit the oedema. Our results suggest that low power laser irradiation possibly exerts its anti-inflammatory effects by stimulating the release of adrenal corticosteroid hormones.

Assuntos

Alumínio , Arseniatos , Carragenina/farmacologia , Edema/induzido quimicamente , Edema/radioterapia , Extremidades/efeitos da radiação , Gálio , Terapia com Luz de Baixa Intensidade , Adrenalectomia , Animais , Diclofenaco/farmacologia , Edema/tratamento farmacológico , Edema/patologia , Extremidades/patologia , Inflamação/induzido quimicamente , Inflamação/patologia , Inflamação/radioterapia , Masculino , Ratos , Ratos Wistar , Fatores de Tempo

RESUMO

O objetivo do presente estudo foi investigar o efeito do laser de baixa potência (LLLT) na hiper-reatividade da traquéia de ratos Wistar macho(RTHR) depois da administração de lipopolissacarídeo (LPS)

Assuntos

Animais , Masculino , Ratos , Lipopolissacarídeos , Terapia com Luz de Baixa Intensidade , Pneumopatias , Cloreto de Metacolina , Pneumonia , Ratos Wistar , Traqueia

RESUMO

Plant extracts have been used for centuries as a popular mode of treatment for several health disorders. Over the last ten years, the study of those extracts has attracted attention in different fields of the biological sciences. Ginger, the rhizome of Zingiber officinale Roscoe (Zingiberaceae), is a commom constituent of diet worldwide and it has been reported that its extracts present some pharmacological activities. Here we investigate the effects of the crude hydralcoholic extract of ginger rhizomes on the classical models of rat paw and skin edema. The carrageenan-, compound 48/80- or serotonin-induced rat paw edema were inhibited significantly by the intraperitoneal administration of alcoholic ginger extract. Ginger extract was also effective in inhibiting 48/80-induced rat skin edema at doses of 0.6 and 1.8 mg/site. Rat skin edema induced by substance P or bradikinin was not affected by treatment with Z. officinalle extract. The intraperitoneal administration of ginger extract (186 mg/kg(-1) body wt.) 1 h prior to serotonin injections, reduced significantly the serotonin-induced rat skin edema. Our results demonstrated that crude extract of Zingiber officinale was able to reduce rat paw and skin edema induced by carrageenan, 48/80 compound and serotonin. The antiedematogenic activity seems to be related, at least partially, to an antagonism of the serotonin receptor.

Assuntos

Anti-Inflamatórios/farmacologia , Edema/tratamento farmacológico , Extratos Vegetais/farmacologia , Rizoma/química , Zingiber officinale/química , Animais , Anti-Inflamatórios/química , Anti-Inflamatórios/uso terapêutico , Edema/induzido quimicamente , Masculino , Extratos Vegetais/química , Plantas Medicinais/química , Ratos , Ratos Wistar , Serotonina/farmacologia , Pele/efeitos dos fármacos , Pele/patologia , p-Metoxi-N-metilfenetilamina/farmacologia

RESUMO

The aqueous fraction of the ethanolic extract (AFL) of Cissampelos sympodialis Eichl (Menispermaceae), popularly known as milona, has been shown to have both immunosuppressive and anti-inflammatory effects. In the present study we investigated the modulation of macrophage antimicrobicidal activity by in vitro treatment with the extract from C. sympodialis. Normal and thioglycolate-elicited mouse peritoneal macrophages were infected in vitro with the protozoan Trypanosoma cruzi DM28c clone. We observed that the AFL (used at doses ranging from 13 to 100 microg/ml) increased T. cruzi growth and induced a 75% reduction in nitric oxide production. This inhibition could be mediated by the stimulation of macrophage interleukin-10 (IL-10) secretion since the in vitro treatment with the AFL stimulated IL-10 production by T. cruzi-infected macrophages. These results suggest that the anti-inflammatory effect of the AFL from C. sympodialis could be, at least in part, mediated by the inhibition of macrophage functions and that the inhibition of macrophage microbicidal activity induced by the C. sympodialis extract may be mediated by the decrease in macrophage function mediated by interleukin-10 production.

Assuntos

Anti-Inflamatórios/farmacologia , Cissampelos/química , Interleucina-10/biossíntese , Macrófagos Peritoneais/efeitos dos fármacos , Extratos Vegetais/farmacologia , Trypanosoma cruzi/efeitos dos fármacos , Animais , Células Cultivadas , Feminino , Ativação de Macrófagos/efeitos dos fármacos , Macrófagos Peritoneais/parasitologia , Macrófagos Peritoneais/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Óxido Nítrico/biossíntese , Folhas de Planta , Trypanosoma cruzi/crescimento & desenvolvimento

RESUMO

The aqueous fraction of the ethanolic extract (AFL) of Cissampelos sympodialis Eichl (Menispermaceae), popularly known as milona, has been shown to have both immunosuppressive and anti-inflammatory effects. In the present study we investigated the modulation of macrophage antimicrobicidal activity by in vitro treatment with the extract from C. sympodialis. Normal and thioglycolate-elicited mouse peritoneal macrophages were infected in vitro with the protozoan Trypanosoma cruzi DM28c clone. We observed that the AFL (used at doses ranging from 13 to 100 æg/ml) increased T. cruzi growth and induced a 75 percent reduction in nitric oxide production. This inhibition could be mediated by the stimulation of macrophage interleukin-10 (IL-10) secretion since the in vitro treatment with the AFL stimulated IL-10 production by T. cruzi-infected macrophages. These results suggest that the anti-inflammatory effect of the AFL from C. sympodialis could be, at least in part, mediated by the inhibition of macrophage functions and that the inhibition of macrophage microbicidal activity induced by the C. sympodialis extract may be mediated by the decrease in macrophage function mediated by interleukin-10 production

Assuntos

Animais , Masculino , Feminino , Camundongos , Anti-Inflamatórios , Cissampelos/química , Interleucina-10 , Macrófagos Peritoneais , Extratos Vegetais , Trypanosoma cruzi , Células Cultivadas , Ativação de Macrófagos , Macrófagos Peritoneais , Camundongos Endogâmicos BALB C , Óxido Nítrico , Folhas de Planta , Trypanosoma cruzi