979 resultados para Expressão de citocinas
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Pós-graduação em Medicina Veterinária - FCAV
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Pós-graduação em Fisioterapia - FCT
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Pós-graduação em Medicina Veterinária - FMVZ
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Pós-graduação em Ciência Animal - FMVA
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Dexamethasone is a synthetic glucocorticoid widely used to treat allergic and inflammatory processes. This drug is used in three main situations, are used to contain acute or chronic inflammatory processes, or like immunosuppressive drug's. In these cases the patient will receive high doses for a chronic period and, therefore, has a much greater chance of adverse side effects, such as hypertension, diabetes and dyslipidemia. Dexamethasone promotes deleterious effects on the arachidonic acid pathway, when administered in high doses, because it is a potent anti-inflammatory drug. We recently demonstrated that dexamethasone significantly reduces the protein expression of vascular endothelial growth factor (VEGF) in both skeletal muscle and heart, but the mechanisms involved remain unclear. Meanwhile, exercise has been shown to be effective against high blood pressure, diabetes and dyslipidemia, promoting, among other factors, the increase in VEGF and angiogenesis. One possible explanation for these effects would be the creation of new vessels mediated by inflammation, or by the stimulation of the formation of products of the metabolism of arachidonic acid (AA), such as prostaglandin E2 (PGE2) and VEGF, by increasing the stimulation of the enzymes cyclooxygenase 1 and 2 (COX-1 and COX-2). Little is known about the preventive effects of training on the action of dexamethasone in the arachidonic acid pathway. Therefore, the aim of this study was to determine whether aerobic exercise training, performed before and concomitant treatment with dexamethasone, was able to prevent the effects of the dexamethasone in the protein expression of COX-2 and VEGF. For this, we used young Wistar rats (n = 40) which were randomly divided into 4 groups: sedentary control (SC), sedentary and treated with dexamethasone (SD), trained control (TC) and trained and treated with dexamethasone (TD). These rats performed aerobic exercise training, 60% of maximum capacity, 5
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Muscle atrophy is always associated with Dexamethasone (Dexa) treatment, however the mechanisms are not completely understood. This study investigated the effects of Dexa on myostatin and p70S6K protein expression and if previous exercise training (T) can attenuate these effects. Eighty rats were distributed into 4 groups: sedentary control (SC), sedentary treated with Dexa (SD; 0,5 mg/kg per day, i.p., 10 days), trained control (TC) and trained treated with Dexa (TD) and underwent a training period where they were either submitted to a running protocol (60% of physical capacity, 5 days/week for 8 weeks) or kept sedentary. After T period, animals underwent Dexa treatment concomitant with training. Western Blot was performed to identify myostatin and p70S6k protein expression in the tibialis anterior (TA) and soleus (SOL) muscle. Ten days of Dexa treatment increased fasting glucose (SD=+62%), however previous T attenuated this increase (TD=+20%, p<0.05). Dexa determined significant decrease in body weight in TD (-22%) and SD (-25%), followed by TA weight reduction in SD (-23%) and TD (-20%). Previous training could not avoid these decreases. Myostatin protein expression was not altered by dexa treatment or training in TA muscle but in SOL muscle it was significantly modified after T, regardless of treatment (TC=+%23 and TD=+25) compared with their respective controls. The protein p70S6K was not modified neither by dexa nor training in any of the analyzed muscle or condition. The results of this study allowed us to conclude that previous training attenuates the hyperglycemia induced by Dexa, however it did not prevent the body or muscle weight reductions. Even in the presence of muscle atrophy, the expression of myostatin and p70S6K do not justify the mechanisms of muscle loss induced by Dexa, which suggests that other catabolic or anabolic proteins could be involved in the process of muscle atrophy after 10 days of treatment with Dexa
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Pós-graduação em Medicina Veterinária - FMVZ
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)