ALESSANDRA CHOQUETA DE TOLEDO ARRUDA
Projetos de Pesquisa
Unidades Organizacionais
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
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conferenceObject Time course effects of exercise training on pulmonary injury induced by exposure to cigarette smoke in mice(2013) TOLEDO-ARRUDA, Alessandra C.; GUARNIER, Flavia; SUEHIRO, Camila L.; ALMEIDA, Francine; OLIVO, Clarice; LOPES, Fernanda; VIEIRA, Rodolfo; CAMARGO-FILHO, Jose Carlos Silva; CECCHINI, Rubens; LIN, Chin; MARTINS, Milton A.conferenceObject Time-Course Effects Of Aerobic Exercise On Lung Mechanics And Inflammation In Mice Exposed To Cigarette Smoke(2013) TOLEDO, A. C.; SUEHIRO, C.; ALMEIDA, F. M.; OLIVO, C.; LOPES, F. D.; VIEIRA, R. P.; LIN, C. J.; MARTINS, M. A.- 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.
- Time-course effects of aerobic physical training in the prevention of cigarette smoke-induced COPD(2017) TOLEDO-ARRUDA, Alessandra C.; VIEIRA, Rodolfo P.; GUARNIER, Flavia A.; SUEHIRO, Camila L.; CALEMAN-NETO, Agostinho; OLIVO, Clarice R.; ARANTES, Petra M. M.; ALMEIDA, Francine M.; LOPES, Fernanda D. T. Q. S.; RAMOS, Ercy M. C.; CECCHINI, Rubens; LIN, Chin Jia; MARTINS, Milton ArrudaA previous study by our group showed that regular exercise training (ET) attenuated pulmonary injury in an experimental model of chronic exposure to cigarette smoke (CS) in mice, but the time-course effects of the mechanisms involved in this protection remain poorly understood. We evaluated the temporal effects of regular ET in an experimental model of chronic CS exposure. Male C57BL/6 mice were divided into four groups: Control (sedentary + air), Exercise (aerobic training + air), Smoke (sedentary + smoke), and Smoke + Exercise (aerobic training + smoke). Mice were exposed to CS and ET for 4, 8, or 12 wk. Exercise protected mice exposed to CS from emphysema and reductions in tissue damping and tissue elastance after 12 wk (P < 0.01). The total number of inflammatory cells in the bronchoalveolar lavage increased in the Smoke group, mainly due to the recruitment of macrophages after 4 wk, neutrophils and lymphocytes after 8 wk, and lymphocytes and macrophages after 12 wk (P < 0.01). Exercise attenuated this increase in mice exposed to CS. The protection conferred by exercise was mainly observed after exercise adaptation. Exercise increased IL-6 and IL-10 in the quadriceps and lungs (P < 0.05) after 12 wk. Total antioxidant capacity and SOD was increased and TNF-alpha and oxidants decreased in lungs of mice exposed to CS after 12 wk (P < 0.05). The protective effects of exercise against lung injury induced by cigarette smoke exposure suggests that anti-inflammatory mediators and antioxidant enzymes play important roles in chronic obstructive pulmonary disease development mainly after the exercise adaptation. NEW & NOTEWORTHY These experiments investigated for the first time the temporal effects of regular moderate exercise training in cigarette smoke-induced chronic obstructive pulmonary disease. We demonstrate that aerobic conditioning had a protective effect in emphysema development induced by cigarette smoke exposure. This effect was most likely secondary to an effect of exercise on oxidant-antioxidant balance and anti-inflammatory mediators.
- A flavanone from Baccharis retusa (Asteraceae) prevents elastase-induced emphysema in mice by regulating NF-kappa B, oxidative stress and metalloproteinases (vol 16, 79, 2015)(2015) TAGUCHI, Laura; PINHEIRO, Nathalia M.; OLIVO, Clarice R.; CHOQUETA-TOLEDO, Alessandra; GRECCO, Simone S.; LOPES, Fernanda D. T. Q. S.; CAPERUTO, Luciana C.; MARTINS, Milton A.; TIBERIO, Iolanda F. L. C.; CAMARA, Niels O.; LAGO, Joao Henrique G.; PRADO, Carla M.
- A flavanone from Baccharis retusa (Asteraceae) prevents elastase-induced emphysema in mice by regulating NF-kappa B, oxidative stress and metalloproteinases(2015) TAGUCHI, Laura; PINHEIRO, Nathalia M.; OLIVO, Clarice R.; CHOQUETA-TOLEDO, Alessandra; GRECCO, Simone S.; LOPES, Fernanda D. T. Q. S.; CAPERUTO, Luciana C.; MARTINS, Milton A.; TIBERIO, Iolanda F. L. C.; CAMARA, Niels O.; LAGO, Joao Henrique G.; PRADO, Carla M.Background: Pulmonary emphysema is characterized by irreversible airflow obstruction, inflammation, oxidative stress imbalance and lung remodeling, resulting in reduced lung function and a lower quality of life. Flavonoids are plant compounds with potential anti-inflammatory and antioxidant effects that have been used in folk medicine. Our aim was to determine whether treatment with sakuranetin, a flavonoid extracted from the aerial parts of Baccharis retusa, interferes with the development of lung emphysema. Methods: Intranasal saline or elastase was administered to mice; the animals were then treated with sakuranetin or vehicle 2 h later and again on days 7, 14 and 28. We evaluated lung function and the inflammatory profile in bronchoalveolar lavage fluid (BALF). The lungs were removed to evaluate alveolar enlargement, extracellular matrix fibers and the expression of MMP-9, MMP-12, TIMP-1, 8-iso-PGF-2 and p65-NF-kappa B in the fixed tissues as well as to evaluate cytokine levels and p65-NF-kappa B protein expression. Results: In the elastase-treated animals, sakuranetin treatment reduced the alveolar enlargement, collagen and elastic fiber deposition and the number of MMP-9- and MMP-12-positive cells but increased TIMP-1 expression. In addition, sakuranetin treatment decreased the inflammation and the levels of TNF-alpha, IL-1 beta and M-CSF in the BALF as well as the levels of NF-kappa B and 8-iso-PGF-2 alpha in the lungs of the elastase-treated animals. However, this treatment did not affect the changes in lung function. Conclusion: These data emphasize the importance of oxidative stress and metalloproteinase imbalance in the development of emphysema and suggest that sakuranetin is a potent candidate that should be further investigated as an emphysema treatment. This compound may be useful for counteracting lung remodeling and oxidative stress and thus attenuating the development of emphysema.
conferenceObject Cigarette Smoke Associated To Diesel Exhaust Particles (dep) In Mice: Synergy Effects(2013) ARANTES, P. M. M.; TOLEDO, A. C.; ALMEIDA, F. M.; OLIVO, C. R.; MAGALHAES, R. M.; ANG, P. L.; FORNAZIEIRO, L. R.; MACCHIONE, M.; SALDIVA, P. H. N.; BISELLI, P. J. C.; LOPES, F. D. T. Q. S.; MARTINS, M. A.article 25 Citação(ões) na Scopus A comparative study of extracellular matrix remodeling in two murine models of emphysema(2013) LOPES, F. D. T. Q. S.; TOLEDO, A. C.; OLIVO, C. R.; PRADO, C. M.; LEICK, E. A.; MEDEIROS, M. C.; SANTOS, A. B. G.; GARIPPO, A.; MARTINS, M. A.; MAUAD, T.A single instillation of porcine pancreatic elastase (PPE) results in significant airspace enlargement on the 28th day after instillation, whereas cigarette smoke (CS) exposure requires 6 months to produce mild emphysema in rodents. Considering that there are differences in the pathogenesis of parenchymal destruction in these different experimental models, it is likely that there may be different patterns of extracellular matrix (ECM) remodeling. To evaluate ECM remodeling, C57BL/6 mice were submitted to either a nasal drop of PPE (PPE 28 Days) or exposed for 6 months to cigarette smoke (CS 6 months). Control groups received either an intranasal instillation of saline solution (Saline 28 Days) or remained without any smoke inhalation for six months (Control 6 months). We measured the mean linear intercept and the volume proportion of collagen type I, collagen type III, elastin and fibrillin. We used emission-scanning confocal microscopy to verify the fiber distribution. Both models induced increased mean linear intercept in relation to the respective controls, being larger in the elastase model in relation to the CS model. In the CS model, emphysema was associated with an increase in the volume proportion of fibrillin, whereas in the PPE model there was an increase in the parenchymal elastin content. In both models, there was an increase in collagen type III, which was higher in the CS-exposed mice. We concluded that ECM remodeling is different in the two most used experimental models of emphysema.