DENISE FREDIANI BARBEIRO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
17 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 17
- Th17/Treg-Related Intracellular Signaling in Patients with Chronic Obstructive Pulmonary Disease: Comparison between Local and Systemic Responses(2021) LOURENCO, Juliana D.; TEODORO, Walcy R.; BARBEIRO, Denise F.; VELOSA, Ana Paula P.; SILVA, Larissa E. F.; KOHLER, Julia B.; MOREIRA, Alyne R.; V, Marcelo Aun; SILVA, Isadora C. da; FERNANDES, Frederico L. A.; NEGRI, Elnara M.; GROSS, Jefferson L.; TIBERIO, Iolanda F. L. C.; ITO, Juliana T.; LOPES, Fernanda D. T. Q. S.Th17/Treg imbalance plays a pivotal role in COPD development and progression. We aimed to assess Th17/Treg-related intracellular signaling at different COPD stages in local and systemic responses. Lung tissue and/or peripheral blood samples were collected and divided into non-obstructed (NOS), COPD stages I and II, and COPD stages III and IV groups. Gene expression of STAT3 and -5, ROR gamma t, Foxp3, interleukin (IL)-6, -17, -10, and TGF-beta was assessed by RT-qPCR. IL-6, -17, -10, and TGF-beta levels were determined by ELISA. We observed increased STAT3, ROR gamma t, Foxp3, IL-6, and TGF-beta gene expression and IL-6 levels in the lungs of COPD I and II patients compared to those of NOS patients. Regarding the systemic response, we observed increased STAT3, ROR gamma t, IL-6, and TGF-beta gene expression in the COPD III and IV group and increased IL-6 levels in the COPD I and II group. STAT5 was increased in COPD III and IV patients, although there was a decrease in Foxp3 expression and IL-10 levels in the COPD I and II and COPD III and IV groups, respectively. We demonstrated that an increase in Th17 intracellular signaling in the lungs precedes this increase in the systemic response, whereas Treg intracellular signaling varies between the compartments analyzed in different COPD stages.
conferenceObject Intestinal Barrier Dysfunction in Ageing Animals With Acute Pancreatitis: Increased Intestinal Inflammation?(2015) MACHADO, Marcel C.; SILVA, Fabiano Pinheiro da; CUNHA, Debora G.; BARBEIRO, Denise F.; COELHO, Ana Maria M.; SOUZA, Heraldo P.- Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice(2021) SERRA, Mariana B.; KOIKE, Marcia K.; BARBEIRO, Denise F.; MACHADO, Marcel C. C.; SOUZA, Heraldo P. deBiliary acute pancreatitis induction by sodium taurocholate infusion has been widely used by the scientific community due to the representation of the human clinical condition and reproduction of inflammatory events corresponding to the onset of clinical biliary pancreatitis. The severity of pancreatic damage can be assessed by measuring the concentration, speed, and volume of the infused bile acid. This study provides an updated checklist of the materials and methods used in the protocol reproduction and shows the main results from this acute pancreatitis (AP) model. Most of the previous publications have limited themselves to reproducing this model in rats. We have applied this method in mice, which provides additional advantages (i.e., the availability of an arsenal of reagents and antibodies for these animals along with the possibility of working with genetically modified strains of mice) that may be relevant to the study. For acute pancreatitis induction in mice, we present a systematic protocol, with a defined dose of 2.5% sodium taurocholate at an infusion speed 10 mu L/min for 3 min in C57BL/6 mice that reaches its maximal level of severity within 12 h of induction and highlight results with outcomes that validate the method. With practice and technique, the total estimated time, from the induction of anesthesia to the completion of the infusion, is 25 min per animal.
conferenceObject Decrease of CC-Family Chemokines Levels in the Heart Tissue of Aged Rats Following Severe Acute Pancreatitis: A New Mechanism of Heart Protection During Systemic Inflammation(2016) AMARAL, Rizia C.; BARBEIRO, Denise F.; KOIKE, Marcia K.; SILVA, Fabiano P.; MACHADO, Marcel C.- Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice(2017) FUSCO, Fernanda B.; GOMES, Diego J.; BISPO, Kely C. S.; TOLEDO, Veronica P.; BARBEIRO, Denise F.; CAPELOZZI, Vera L.; FURUKAWA, Luzia N. S.; VELOSA, Ana P. P.; TEODORO, Walcy R.; HEIMANN, Joel C.; QUINTAO, Eder C. R.; PASSARELLI, Marisa; NAKANDAKARE, Edna R.; CATANOZI, SergioThis study investigated the influence of sodium restriction and antihypertensive drugs on atherogenesis utilizing hypertensive (H) low-density lipoprotein-receptor knockout mice treated or not with losartan (Los) or hydralazine (Hyd) and fed low-sodium (LS) or normal-sodium (NS) chow. Despite reducing the blood pressure (BP) of H-LS mice, the LS diet caused arterial lipid infiltration due to increased plasma total cholesterol (TC) and triglycerides (TG). Los and Hyd reduced the BP of H-LS mice, and Los effectively prevented arterial injury, likely by reducing plasma TG and nonesterified fatty acids. Aortic lipid infiltration was lower in Los-treated H-LS mice (H-LS+Los) than in normotensive (N)-LS and H-LS mice. Aortic angiotensin II type 1 (AT1) receptor content was greater in H-NS than H-LS mice and in H-LS+Hyd than H-LS+Los mice. Carboxymethyl-lysine (CML) and receptor for advanced glycation end products (RAGE) immunostaining was greater in H-LS than H-NS mice. CML and RAGE levels were lower in LS animals treated with antihypertensive drugs, and Hyd enhanced the AT1 receptor level. Hyd also increased the gene expression of F4/80 but not tumor necrosis factor-a, interleukin (IL)-1 beta, IL-6, IL-10, intercellular adhesion molecule-1 or cluster of differentiation 66. The novelty of the current study is that in a murine model of simultaneous hypertension and hyperlipidemia, the pleiotropic effect of chronic, severe sodium restriction elicited aortic damage even with reduced BP. These negative effects on the arterial wall were reduced by AT1 receptor antagonism, demonstrating the influence of angiotensin II in atherogenesis induced by a severely LS diet.
- Low level laser therapy reduces acute lung inflammation without impairing lung function(2016) CURY, Vivian; LIMA, Thais Martins de; PRADO, Carla Maximo; PINHEIRO, Nathalia; ARIGA, Suely K. K.; BARBEIRO, Denise F.; MORETTI, Ana I.; SOUZA, Heraldo P.Acute lung injury is a condition characterized by exacerbate inflammatory reaction in distal airways and lung dysfunction. Here we investigate the treatment of acute lung injury (ALI) by low level laser therapy (LLLT), an effective therapy used for the treatment of patients with inflammatory disorders or traumatic injuries, due to its ability to reduce inflammation and promote tissue regeneration. However, studies in internal viscera remains unclear. C57BL/6 mice were treated with intratracheal lipopolysaccharide (LPS) (5 mg/kg) or phosphate buffer saline (PBS). Six hours after instillation, two groups were irradiated with laser at 660 nm and radiant exposure of 10 J/cm(2). Intratracheal LPS inoculation induced a marked increase in the number of inflammatory cells in perivascular and alveolar spaces. There was also an increase in the expression and secretion of cytokines (TNF-alpha, IL-1 beta, IL-6,) and chemokine (MCP-1). The LLLT application induced a significant decrease in both inflammatory cells influx [GRAPHICS] and inflammatory mediators secretion. These effects did not affect lung mechanical properties, since no change was observed in tissue resistance or elastance. In conclusion LLLT is able to reduce inflammatory reaction in lungs exposed to LPS without affecting the pulmonary function and recovery.
conferenceObject Urinary NGAL biomarker predicts non response to therapy with albumin and terlipressin in patients with hepatorenal syndrome(2016) XIMENES, Rafael O.; HELOU, Claudia; BARBEIRO, Denise F.; SOUZA, Heraldo; MIGITA, Beatriz; D'ALBUQUERQUE, Luiz C.; CARRILHO, Flair J.; FARIAS, Alberto O.- BONE MARROW CELLS TRANSPLANT IN SEPTIC MICE MODULATES SYSTEMIC INFLAMMATORY RESPONSE VIA CELL-CELL CONTACT(2019) LORIGADOS, Clara B.; ARIGA, Suely K. K.; LIMA, Thais M. de; BARBEIRO, Denise F.; KRIEGER, Jose E.; SORIANO, Francisco G.Sepsis is a dynamic disease, displaying an inflammatory profile that varies over time and for each organ. Controlling the inflammatory response based in targeting a single molecule has been proved useless. We hypothesized that treatment with bone marrow-derived mononuclear cells (BMDMCs) may be more efficient to modulate the systemic inflammatory response to infection. Adult male Balb/c mice were subjected to cecal ligation and puncture (CLP) or endotoxemia model of experimental sepsis. BMDMCs were separated under Ficoll gradient and injected intravenously 1 h after the procedures. Cytokines concentration was quantified in plasma, lungs, heart, and gut. Spleens, lymph nodes, and thymus were used for lymphocytes isolation and cell death assessment. All measurements were performed 2 h after BMDMCs injection. RAW264.7 macrophages and BMDMCs were cocultivated in vitro to investigate the mechanisms involved. Our data showed that an early single intravenous injection of BMDMCs in animals submitted to the murine model of endotoxemia led to the improvement of survival rate; BMDMCs persistency in lung, liver, and spleen after 24 h; decreased necrosis and apoptosis of mononuclear cells; lower TNF-a, but increased IL-10 concentration in plasma; and tissue-specific cytokine profile. In vitro experiments demonstrated that IL-6, IL-10, and nitric oxide production depends on direct contact of BMDMCs to macrophages and that TNF-a production is negatively regulated by PGE2. BMDMCs are efficient in protecting animals from endotoxemia and sepsis, reducing systemic inflammation as well as specifically modulating tissue inflammation, producing the necessary immune regulation to re-equilibrate the inflammatory response.
conferenceObject PEQUI FRUIT (CARYOCAR BRASILIENSE CAMB) PULP OIL, A NATURAL SOURCE OF ANTIOXIDANTS, REDUCE THE OXIDATIVE STRESS STATUS AND DNA DAMAGE IN EXPERIMENTAL LUNG CANCER(2012) COLOMBO, Natalia B. R.; PARRA, Edwin R.; GRISOLIA, Cesar K.; GELAIN, Daniel P.; HAGE, Marcia; SCHNORR, Carlos E.; KOLLING, Eduardo; BARBEIRO, Denise F.; CAPELOZZI, Vera L.Background: It is well known that the endogenous antioxidant enzyme defense as well as an adequate ingestion of exogenous sources of antioxidants prevents the oxidative damage caused by reactive species (ROS),including DNA damage, and can reduce the risk of cancer, atherosclerosis and other degenerative diseases. The pulp of Caryocar brasiliense Camb, most known as pequi, is a Brazilian fruit that has high levels of antioxidants properties, such as vitamin C, carotenoids, phenolic compounds like flavonoids, saponins and tannins, and essential oils. The aim of this study was to estimate and to evaluate the antioxidant enzyme activities of catalase (CAT) and superoxide dismutase (SOD), as well as the ratio between then, and the antioxidant activity of the pequi oil, measuring lipid peroxidation and DNA damage in experimental model of lung cancer induced by urethane. Methods: The study was performed in 18 male BALB/c mice: 14 animals received by gavage 0,5μL/mg/day of pequi oil (PI0601631-6) (Control+CBCoil = 4) during 75 days. After 15 days of the beginning of the gavage, 10 of these mices received two doses of 1,5g/kg intraperitoneal of urethane (Urethane+CBC oil=10). The other 4 animals were only submitted to two doses of 1,5g/kg intraperitoneal of urethane (Urethane group=4). After 75 days, the three groups were sacrificed. The antioxidant activity of pequi oil was evaluated in the lung tissues by the biochemical TBARS (Thiobarbituric acidreactive substances), CAT and SOD test. The DNA damage was estimated by the comet test method. Results and Conclusion: The lung parenchyma from the Urethane groups without oil and with oil showed neoplasic formations induced by the chemical carcinogenesis in contrast with Control + CBC oil group. The results of the TBARS test showed a significant decreased of the lipid peroxidation in the Urethane + CBC oil, similar as values of the Control+CBC oil, when compared with Urethane group. The CAT and SOD test, as well as the ratio between then, didn’t show a significant difference. The image analysis of the comet assay showed a statistical significant decreased of the DNA damage cells in the Urethane + CBC oil group when compared with urethane group (p=0.001). The decreased DNA damage was very similar that we obtained in the Control + CBC oil group. We conclude that the different natural antioxidant components found in the pequi oil are efficient to diminish the oxidative stress status and the DNA damage in chemical carcinogenesis induced by urethane experimental lung cancer, suggesting that this type of strategies may have a greater impact in lung cancer treatment.- Chemical Characterization and Wound Healing Property of Jacaranda decurrens Cham. (Bignoniaceae): An Experimental Study Based on Molecular Mechanisms(2020) SERRA, Mariana B.; BARROSO, Wermerson A.; ROCHA, Claudia; FURTADO, Pablo G. R.; BORGES, Antonio C. R.; SILVA, Selma N.; TANGERINA, Marcelo M. P.; NASCIMENTO, Jessyane R. do; VILEGAS, Wagner; ALVES, Ademilton C.; BARBEIRO, Denise F.; SOUZA, Heraldo P. de; ABREU, Iracelle C.; BORGES, Marilene O. R.Background. Jacaranda decurrens Cham., known as carobinha, is prevalent in the Cerrado biome and presents popular use in treatment of dermatological diseases. The present study aimed to investigate the healing action of topical formulation of Jacaranda decurrens Cham. (FtEHJ) in mice cutaneous lesions. Methods. Phytochemical analysis of J. decurrens hydroalcoholic extract was carried out by using HPLC-PDA-ESI-MS and FIA-ESI-IT-MSn. Swiss mice were treated topically with formulation base (FtB) or Fibrinase (R) or ointment FtEHJ (15 mg/g; 50 mg/Kg). At the end of treatment periods, the inflammatory cytokines (TNF-alpha, IL-1 beta, and IL-6) in the lesions were measured by using ELISA and gene expression of TGF-beta, Collagen I, and Collagen III was demonstrated by RTqPCR method and histological evaluation. Results. Ten compounds were identified in the extract, distributed among the classes of flavonoids and triterpenes. Treatment with FtEHJ increased the wound contraction in 24 hours, such as reduction of TNF-alpha, IL-1 beta, and IL-6 (pg/mL) cytokines in the lesion. The TGF-beta and collagen gene expression was increased and the wound closure accelerated to nine days, with discrete inflammation, collagenization, and accented reepithelialization. Conclusions. The results obtained suggest chemical compounds present in the FtEHJ accelerates wound healing by being a gene expression modulator, and protein content of different molecules are involved in tissue repair.