FERNANDA DEGOBBI TENORIO QUIRINO DOS SANTOS LOPES
Projetos de Pesquisa
Unidades Organizacionais
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
9 resultados
Resultados de Busca
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- Aerobic exercise attenuates pulmonary injury induced by exposure to cigarette smoke(2012) TOLEDO, A. C.; MAGALHAES, R. M.; HIZUME, D. C.; VIEIRA, R. P.; BISELLI, P. J. C.; MORIYA, H. T.; MAUAD, T.; LOPES, F. D. T. Q. S.; MARTINS, M. A.It has recently been suggested that regular exercise reduces lung function decline and risk of chronic obstructive pulmonary disease (COPD) among active smokers; however, the mechanisms involved in this effect remain poorly understood. The present study evaluated the effects of regular exercise training in an experimental mouse model of chronic cigarette smoke exposure. Male C57BL/6 mice were divided into four groups (control, exercise, smoke and smoke+exercise). For 24 weeks, we measured respiratory mechanics, mean linear intercept, inflammatory cells and reactive oxygen species (ROS) in bronchoalveolar lavage (BAL) fluid, collagen deposition in alveolar walls, and the expression of antioxidant enzymes, matrix metalloproteinase 9, tissue inhibitor of metalloproteinase (TIMP) 1, interleukin (IL)-10 and 8-isoprostane in alveolar walls. Exercise attenuated the decrease in pulmonary elastance (p<0.01) and the increase in mean linear intercept (p=0.003) induced by cigarette smoke exposure. Exercise substantially inhibited the increase in ROS in BAL fluid and 8-isoprostane expression in lung tissue induced by cigarette smoke. In addition, exercise significantly inhibited the decreases in IL-10, TIMP1 and CuZn superoxide dismutase induced by exposure to cigarette smoke. Exercise also increased the number of cells expressing glutathione peroxidase. Our results suggest that regular aerobic physical training of moderate intensity attenuates the development of pulmonary disease induced by cigarette smoke exposure.
- N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation(2012) CAMPOS, Renata; SHIMIZU, Maria Heloisa Massola; VOLPINI, Rildo Aparecido; BRAGANCA, Ana Carolina de; ANDRADE, Lucia; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; OLIVO, Clarice; CANALE, Daniele; SEGURO, Antonio CarlosCampos R, Shimizu MH, Volpini RA, de Bragan a AC, Andrade L, Lopes FD, Olivo C, Canale D, Seguro AC. N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation. Am J Physiol Lung Cell Mol Physiol 302: L640-L650, 2012. First published January 20, 2012; doi: 10.1152/ajplung.00097.2011.-Sepsis is a common cause of acute kidney injury (AKI) and acute lung injury. Oxidative stress plays as important role in such injury. The aim of this study was to evaluate the effects that the potent antioxidant N-acetylcysteine (NAC) has on renal and pulmonary function in rats with sepsis. Rats, treated or not with NAC (4.8 g/l in drinking water), underwent cecal ligation and puncture (CLP) 2 days after the initiation of NAC treatment, which was maintained throughout the study. At 24 h post-CLP, renal and pulmonary function were studied in four groups: control, control + NAC, CLP, and CLP + NAC. All animals were submitted to low-tidal-volume mechanical ventilation. We evaluated respiratory mechanics, the sodium cotransporters Na-K-2Cl (NKCC1) and the alpha-subunit of the epithelial sodium channel (alpha-ENaC), polymorphonuclear neutrophils, the edema index, oxidative stress (plasma thiobarbituric acid reactive substances and lung tissue 8-isoprostane), and glomerular filtration rate. The CLP rats developed AKI, which was ameliorated in the CLP + NAC rats. Sepsis-induced alterations in respiratory mechanics were also ameliorated by NAC. Edema indexes were lower in the CLP + NAC group, as was the wet-to-dry lung weight ratio. In CLP + NAC rats, alpha-ENaC expression was upregulated, whereas that of NKCC1 was downregulated, although the difference was not significant. In the CLP + NAC group, oxidative stress was significantly lower and survival rates were significantly higher than in the CLP group. The protective effects of NAC (against kidney and lung injury) are likely attributable to the decrease in oxidative stress, suggesting that NAC can be useful in the treatment of sepsis.
- Anti-inflammatory Effects of Aerobic Exercise in Mice Exposed to Air Pollution(2012) VIEIRA, Rodolfo de Paula; TOLEDO, Alessandra Choqueta; SILVA, Lucas Bogaz; ALMEIDA, Francine Maria; DAMACENO-RODRIGUES, Nilsa Regina; CALDINI, Elia Garcia; SANTOS, Angela Batista Gomes; RIVERO, Dolores Helena; HIZUME, Deborah Camargo; LOPES, Fernanda Degobbi Tenorio Quirino Santos; OLIVO, Clarice Rosa; CASTRO-FARIA-NETO, Hugo Caire; MARTINS, Milton Arruda; SALDIVA, Paulo Hilario Nascimento; DOLHNIKOFF, MarisaPurpose: Exposure to diesel exhaust particles (DEP) results in lung inflammation. Regular aerobic exercise improves the inflammatory status in different pulmonary diseases. However, the effects of long-term aerobic exercise on the pulmonary response to DEP have not been investigated. The present study evaluated the effect of aerobic conditioning on the pulmonary inflammatory and oxidative responses of mice exposed to DEP. Methods: BALB/c mice were subjected to aerobic exercise five times per week for 5 wk, concomitantly with exposure to DEP (3 mg.mL (1); 10 mu L per mouse). The levels of exhaled nitric oxide, reactive oxygen species, cellularity, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were analyzed in bronchoalveolar lavage fluid, and the density of neutrophils and the volume proportion of collagen fibers were measured in the lung parenchyma. The cellular density of leukocytes expressing IL-1 beta, keratinocyte chemoattractant (KC), and TNF-alpha in lung parenchyma was evaluated with immunohistochemistry. The levels of IL-1 beta, KC, and TNF-alpha were also evaluated in the serum. Results: Aerobic exercise inhibited the DEP-induced increase in the levels of reactive oxygen species (P < 0.05); exhaled nitric oxide (P < 0.01); total (P < 0.01) and differential cells (P < 0.01); IL-6 and TNF-alpha levels in bronchoalveolar lavage fluid (P < 0.05); the level of neutrophils (P < 0.001); collagen density in the lung parenchyma (P < 0.05); the levels of IL-6, KC, and TNF-alpha in plasma (P < 0.05); and the expression of IL-1 beta, KC, and TNF-alpha by leukocytes in the lung parenchyma (P < 0.01). Conclusions: We conclude that long-term aerobic exercise presents protective effects in a mouse model of DEP-induced lung inflammation. Our results indicate a need for human studies that evaluate the pulmonary responses to aerobic exercise chronically performed in polluted areas.
- Protective effects of aerobic exercise on acute lung injury induced by LPS in mice(2012) GONCALVES, Cintia Tokio Reis; GONCALVES, Carlos Gustavo Reis; ALMEIDA, Francine Maria de; LOPES, Fernanda Degobi Tenorio Quirino dos Santos; DURAO, Ana Carolina Cardoso dos Santos; SANTOS, Fabiana Almeida dos; SILVA, Luiz Fernando Ferraz da; MARCOURAKIS, Tania; CASTRO-FARIA-NETO, Hugo C.; VIEIRA, Rodolfo de Paula; DOLHNIKOFF, MarisaIntroduction: The regular practice of physical exercise has been associated with beneficial effects on various pulmonary conditions. We investigated the mechanisms involved in the protective effect of exercise in a model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Methods: Mice were divided into four groups: Control (CTR), Exercise (Exe), LPS, and Exercise + LPS (Exe + LPS). Exercised mice were trained using low intensity daily exercise for five weeks. LPS and Exe + LPS mice received 200 mu g of LPS intratracheally 48 hours after the last physical test. We measured exhaled nitric oxide (eNO); respiratory mechanics; neutrophil density in lung tissue; protein leakage; bronchoalveolar lavage fluid (BALF) cell counts; cytokine levels in BALF, plasma and lung tissue; antioxidant activity in lung tissue; and tissue expression of glucocorticoid receptors (Gre). Results: LPS instillation resulted in increased eNO, neutrophils in BALF and tissue, pulmonary resistance and elastance, protein leakage, TNF-alpha in lung tissue, plasma levels of IL-6 and IL-10, and IL-1beta, IL-6 and KC levels in BALF compared to CTR (P <= 0.02). Aerobic exercise resulted in decreases in eNO levels, neutrophil density and TNF-alpha expression in lung tissue, pulmonary resistance and elastance, and increased the levels of IL-6, IL-10, superoxide dismutase (SOD-2) and Gre in lung tissue and IL-1beta in BALF compared to the LPS group (P <= 0.04). Conclusions: Aerobic exercise plays important roles in protecting the lungs from the inflammatory effects of LPS-induced ALI. The effects of exercise are mainly mediated by the expression of anti-inflammatory cytokines and antioxidants, suggesting that exercise can modulate the inflammatory-anti-inflammatory and the oxidative-antioxidative balance in the early phase of ALI.
conferenceObject A single dose of a specific serinoprotease inhibitor attenuated the protease-antiprotease imbalance in an experimental model of emphysema(2012) OLIVO, Clarice R.; LOURENCO, Juliana D.; NEVES, Luana; ALMEIDA, Francine; PRADO, Carla M.; TIBERIO, Iolanda C. L.; TANAKA, Aparecida; SASAKI, Sergio; MARTINS, Milton A.; LOPES, Fernanda D. T. Q. S.conferenceObject Reduction of endogenous acetylcholine contributes to pulmonary inflammation in a model of emphysema in mice(2012) BANZATO, Rosana; PINHEIRO, Nathalia; OLIVO, Clarice; SANTANA, Fernanda; TIBERIO, Iolanda; PRADO, Vania; PRADO, Marco Antonio; MARTINS, Milton; LOPES, Fernanda; PRADO, CarlaconferenceObject Treatment with proteinase inhibitor, BbCI, modulates inflammatory response, mechanic alterations, and remodeling on elastase-induced emphysema in mice(2012) ALMEIDA-REIS, Rafael; OLIVEIRA, Bruno T. M.; THEODORO-JUNIOR, Osmar A.; OLIVA, Leandro V.; PINHEIRO, Nathalia; BRITO, Marlon V.; LOPES, Fernanda D. Q. T.; PRADO, Carla M.; MARTINS, Milton A.; OLIVA, Maria Luiza V.; TIBERIO, Iolanda F. L. C.conferenceObject Creatine supplementation attenuates systemic and pulmonary effects of acute lung injury induced by pulmonary ischemia-reperfusion in rats(2012) ALMEIDA, Francine; PAZETTI, Rogerio; LOPES, Fernanda Degobbi Tenorio Quirino Santos; SOTO, Sonia Fatima; MARTINS, Milton Arruda; DOLHNIKOFF, Marisa; VIEIRA, Rodolfo PaulaconferenceObject Study of compensatory lung growth after right bilobectomy in a COPD experimental model(2012) ALMEIDA, Francine; SARAIVA-ROMANHOLO, Beatriz; VIEIRA, Rodolfo; MORIYA, Henrique; LOPES, Fernanda; MAUAD, Thais; MARTINS, Milton; PAZETTI, Rogerio