Mecanismos neuroprotetores do exercício físico envolvendo a liberação de Glutamato e a apoteose celular

• Ano de defesa: 2010
• Autor(a) principal: Flavio Afonso Goncalves Mourao
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Fisiologia e Farmacologia; Agentes neuroprotetores; Exercícios físicos Fisiologia; Isquemia cerebral; Acido glutamico Fisiologia; Privação de oxigênio e glicose; Fisiologia; Apoptose
• Link de acesso: http://hdl.handle.net/1843/BUOS-8DPFWJ

Physical activity and its positive effects on health and rehabilitation have been studied over the last few years, to investigate the molecular and physiological protective mechanisms of the physical exercise, taking advantage of controlled and standardized protocols. Studies concerning the protective effects of the physical exercise over highly incident pathologies on the central nervous system have been evidenced. However, molecular mechanisms underlying these effects are still contradictory and poorly explored. Therefore, owing to the fast growth of studies in this area, which mainly uses controlled and standardized animal models of physical exercise, the aim of this work was to analyze neuroprotective mechanisms, involved in glutamate release and cellular apoptosis, after oxygen and glucose deprivation (in vitro ischemia), in cerebral slices of rats submitted to a chronic swimming exercise program. Animals were divided in two groups: exercise and sedentary. The exercise group underwent swimming for eight weeks, while the sedentary group was submitted to the same experimental conditions without having to make swimming exercise program. During and in the end of the exercise period, adaptive characteristics of the animals to effort, stress/emotional state and learning/memory were evaluated. In the end of the evaluations of adaptive physiological characteristics, cerebral slices were submitted to an oxygen and glucose deprivation protocol, in order to analyze the glutamate release, the expression of apoptotic proteins such as caspase-3, -8, -9 and apoptosis-inducing factor, and cellular viability. According to our results animals showed a significant and beneficial adaptive response to the proposed protocol. After the ischemic insult, glutamate release and expression of apoptotic proteins were significantly lower when compared to the sedentary group, while cellular viability was substantially higher in the former. In summary, our results are in accordance with the literature regarding the beneficial and protective effects of exercise, pointing to possible pathways intrinsic to brain structures that adaptively could be modulated, assuring neuroprotection to brain ischemic insults.