CAMILA LIYOKO SUEHIRO
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- The tick-derived rBmTI-A protease inhibitor attenuates the histological and functional changes induced by cigarette smoke exposure(2018) LOURENCO, Juliana D.; ITO, Juliana T.; CERVILHA, Daniela A. B.; SALES, Davi S.; RIANI, Alyne; SUEHIRO, Camila L.; GENARO, Isabella S.; DURAN, Adriana; PUZER, Luciano; MARTINS, Milton A.; SASAKI, Sergio D.; LOPES, Fernanda D. T. Q. S.Introduction. Smoking is the main risk factor for chronic obstructive pulmonary disease development and cigarette smoke (CS) exposure is considered an important approach to reproduce in rodents this human disease. We have previously shown that in an elastase induced model of emphysema, the administration of a protease inhibitor (rBmTI-A) prevented and attenuated tissue destruction in mice. Thus, in this study we aimed to verify the effects of rBmTI-A administration on the physiopathological mechanisms of CS induced emphysema. Methods. Mice (C57BL/6) were exposed to CS or room air for 12 weeks. In this period, 3 nasal instillations of rBmTI-A inhibitor or its vehicle were performed. After euthanasia, respiratory mechanics were evaluated and lungs removed for analysis of mean linear intercept, volume proportion of collagen and elastic fibers, density of polymorphonuclear cells, macrophages, and density of positive cells for MMP-12, MMP-9, TIMP-1 and gp91phox. Results. The rBmTI-A administration improved tissue elastance, decreased alveolar enlargement and collagen fibers accumulation to control levels and attenuated elastic fibers accumulation in animals exposed to CS. There was an increase of MMP-12, MMP-9 and macrophages in CS groups and the rBmTIA only decreased the number of MMP-12 positive cells. Also, we demonstrated an increase in gp91phox in CS treated group and in TIMP-1 levels in both rBmTI-A treated groups. Conclusion. In summary, the rBmTI-A administration attenuated emphysema development by an increase of gp91phox and TIMP-1, accompanied by a decrease in MMP-12 levels.
- Aerobic exercise modulates cardiac NAD(P)H oxidase and the NRF2/KEAP1 pathway in a mouse model of chronic fructose consumption(2020) ALVES, Renata; SUEHIRO, Camila Liyoko; OLIVEIRA, Flavia Garcia de; FRANTZ, Eliete Dalla Corte; MEDEIROS, Renata Frauches de; VIEIRA, Rodolfo de Paula; MARTINS, Milton de Arruda; LIN, Chin Jia; NOBREGA, Antonio Claudio Lucas da; TOLEDO-ARRUDA, Alessandra Choqueta deThe present study investigated the effects of exercise on the cardiac nuclear factor (erythroid-derived 2) factor 2 (NRF2)/Kelch-like ECU-associated protein 1 (KEAP1) pathway in an experimental model of chronic fructose consumption. Male C57BL/6 mice were assigned to Control, Fructose (20% fructose in drinking water), Exercise (treadmill exercise at moderate intensity), and Fructose + Exercise groups (n = 10). After 12 wk. the energy intake and body weight in the groups were similar. Maximum exercise testing, resting energy expenditure, resting oxygen consumption, and carbon dioxide production increased in the exercise groups (Exercise and Fructose + Exercise vs. Control and Fructose groups. P < 0.05). Chronic fructose intake induced circulating hypercholesterolemia, hypertriglyceridemia. and hyperleptinemia and increased white adipose tissue depots, with no changes in blood pressure. This metabolic environment increased circulating IL-6, IL-1 beta, IL-10, cardiac hypertrophy. and cardiac NF-kappa B-p65 and TNF-alpha expression, which were reduced by exercise (P < 0.05). Cardiac ANC. II type 1 receptor and NiD(P)H oxidase 2 (NOX2) were increased by fructose intake and exercise decreased this response (P < 0.05). Exercise increased the cardiac expression of the NRF2-to-KEAP1 ratio and phase II antioxidants in fructose-fed mice (P < 0.05). NOX4, glutathione reductase, and catalase protein expression were similar between the groups. These findings suggest that exercise confers modulatory cardiac effects, improving antioxidant defenses through the NRF2/KEAP1 pathway and decreasing oxidative stress, representing a potential nonpharmacological approach to protect against fructose-induced cardiometabolic diseases. NEW & NOTEWORTHY This is the first study to evaluate the cardiac modulation of NAD(P)H oxidase (NOX), the NRF2/Kelchlike ECH-associated protein 1 pathway (KEAP), and the thioredoxin TRX1) system through exercise in the presence of moderate fructose intake. We demonstrated a novel mechanism by which exercise improves cardiac antioxidant defenses in an experimental model of chronic fructose intake, which involves NRF2-to-KEAP1 ratio modulation, enhancing the local phase II antioxidants hemoxygenase-1, thioredoxin reductase (TXNRD1), and peroxiredoxin1B (PDRX1), and inhibiting cardiac NOX2 overexpression.
- A possible association between fructose consumption and pulmonary emphysema (vol 9, 9344, 2019)(2020) SUEHIRO, Camila Liyoko; TOLEDO-ARRUDA, Alessandra Choqueta de; VIEIRA, Rodolfo de Paula; ALMEIDA, Francine Maria de; OLIVO, Clarice Rosa; MARTINS, Milton de Arruda; LIN, Chin Jia
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.- High fructose intake increases alveolar enlargement and muscle inflammation in mice exposed to cigarette smoke(2016) SUEHIRO, Camila; TOLEDO-ARRUDA, Alessandra; ALMEIDA, Francine; OLIVO, Clarice; OLIVEIRA JR., Manoel; SOUSA, Adilson; VIEIRA, Rodolfo; MARTINS, Milton; LIN, Chin
conferenceObject Aerobic Exercise Attenuates Skeletal Muscle Injury Induced By Cigarette Smoke Exposure In Mice(2014) TOLEDO-ARRUDA, A. C.; SUEHIRO, C. L.; GUARNIER, F. A.; VIEIRA, R. D. P.; ALMEIDA, F. M.; LOPES, F. D.; ARANTES, P. D. M. M.; CECCHINI, R.; LIN, C. J.; MARTINS, M. D. A.- A possible association between fructose consumption and pulmonary emphysema(2019) SUEHIRO, Camila Liyoko; TOLEDO-ARRUDA, Alessandra Choqueta de; VIEIRA, Rodolfo de Paula; ALMEIDA, Francine Maria de; OLIVO, Clarice Rosa; MARTINS, Milton de Arruda; LIN, Chin JiaChronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. In addition to persistent airflow limitation and respiratory symptoms, COPD is also characterized by chronic systemic inflammation. Epidemiological studies have shown that dietary fibers, fruits and vegetables intake protects against the COPD development, while fructose-loading is associated with increased risk of asthma and chronic bronchitis. Since dietary factors might affect susceptibility to COPD by modulating oxidative stress and inflammatory responses, we evaluated how fructose feeding might affect the smoking-induced emphysema in mice. We found that chronic fructose intake induced destruction and remodeling of lung parenchyma and impairment of respiratory mechanics, which are associated with distinctive cytokine profiles in bronchoalveolar lavage fluid, blood plasma and skeletal muscle. The combined effects of chronic fructose intake and cigarette smoking on destruction of lung parenchyma are more pronounced than the effects of either alone. Excessive intake of fructose might directly cause pulmonary emphysema in mice rather than just altering its natural history by facilitating the installation of a low-grade systemic inflammatory milieu.
- 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.
- Aerobic exercise training attenuates detrimental effects of cigarette smoke exposure on peripheral muscle through stimulation of the Nrf2 pathway and cytokines: a time-course study in mice(2020) TOLEDO-ARRUDA, Alessandra C.; SOUSA NETO, Ivo Vieira de; VIEIRA, Rodolfo P.; GUARNIER, Flavia A.; CALEMAN-NETO, Agostinho; SUEHIRO, Camila L.; OLIVO, Clarice R.; CECCHINI, Rubens; PRADO, Carla M.; LIN, Chin J.; DURIGAN, Joao Luiz Quaglioti; MARTINS, Milton A.Cigarette smoke (CS) exposure reduces skeletal muscle function; however, the mechanisms involved have been poorly investigated. The current study evaluated the temporal effects of aerobic exercise training on oxidant and antioxidant systems as well as inflammatory markers in skeletal muscle of mice exposed to CS. Mice were randomly allocated to control, exercise, smoke, and smoke+exercise groups and 3 time points (4, 8, and 12 weeks; n = 12 per group). Exercise training and CS exposure were performed for 30 min/day, twice a day, 5 days/week for 4, 8, and 12 weeks. Aerobic exercise improved functional capacity and attenuated the increase in the cachexia index induced by CS exposure after 12 weeks. Concomitantly, exercise training downregulated tumor necrosis factor a concentration, glutathione oxidation, and messenger RNA (mRNA) expression of Keap1 (P < 0.01) and upregulated interleukin 10 concentration, total antioxidant capacity, and mRNA expression of Nrf2, Gsr, and Txn1 (P < 0.01) in muscle. Exercise increased mRNA expression of Hmox1 compared with the control after 12 weeks (P < 0.05). There were no significant differences between smoke groups for superoxide dismutase activity and Hmox1 mRNA expression. Exercise training improved the ability of skeletal muscle to adequately upregulate key antioxidant and anti-inflammatory defenses to detoxify electrophilic compounds induced by CS exposure, and these effects were more pronounced after 12 weeks. Novelty Exercise attenuates oxidative stress in skeletal muscle from animals exposed to CS via Nrf2 and glutathione pathways. Exercise is a helpful tool to control the inflammatory balance in skeletal muscle from animals exposed to CS. These beneficial effects were evident after 12 weeks.
- Exercise Prevents Diaphragm Wasting Induced by Cigarette Smoke through Modulation of Antioxidant Genes and Metalloproteinases(2018) RAMOS, Gracielle Vieira; TOLEDO-ARRUDA, Alessandra Choqueta de; PINHEIRO-DARDIS, Clara Maria; SUEHIRO, Camila Liyoko; RUSSO, Thiago Luiz de; VIEIRA, Rodolfo Paula; MARTINS, Milton Arruda; SALVINI, Tania Fatima; DURIGAN, Joao Luiz QuagliottiBackground. The present study aimed to analyze the effects of physical training on an antioxidant canonical pathway and metalloproteinases activity in diaphragm muscle in a model of cigarette smoke-induced chronic obstructive pulmonary disease (COPD). Methods. Male mice were randomized into control, smoke, exercise, and exercise + smoke groups, which were maintained in trial period of 24 weeks. Gene expression of kelch-like ECH-associated protein 1; nuclear factor erythroid-2 like 2; and heme-oxygenase1 by polymerase chain reaction was performed. Metalloproteinases 2 and 9 activities were analyzed by zymography. Exercise capacity was evaluated by treadmill exercise test before and after the protocol. Results. Aerobic training inhibited diaphragm muscle wasting induced by cigarette smoke exposure. This inhibition was associated with improved aerobic capacity in those animals that were submitted to 24 weeks of aerobic training, when compared to the control and smoke groups, which were not submitted to training. The aerobic training also downregulated the increase of matrix metalloproteinases (MMP-2 and MMP-9) and upregulated antioxidant genes, such as nuclear factor erythroid-2 like 2 (NRF2) and heme-oxygenase1 (HMOX1), in exercise + smoke group compared to smoke group. Conclusions. Treadmill aerobic training protects diaphragm muscle wasting induced by cigarette smoke exposure involving upregulation of antioxidant genes and downregulation of matrix metalloproteinases.