CAMILA LIYOKO SUEHIRO
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- 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
- 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.
- 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.