CHIN JIA LIN
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/22 - Laboratório de Patolologia Cardiovascular, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/22 - Laboratório de Patolologia Cardiovascular, Hospital das Clínicas, Faculdade de Medicina - Líder
5 resultados
Resultados de Busca
Agora exibindo 1 - 5 de 5
- 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.
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 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.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.- 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.