Avaliação de parâmetros inflamatórios e de estresse oxidativo em cérebros de camundongos após indução de obesidade

• Ano de defesa: 2016
• Autor(a) principal: Souza, Luana da Rosa
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Indução de obesidade; Obesidade; Inflamação; Estresse oxidativo; Cérebro
• Link de acesso: https://repositorio.animaeducacao.com.br/handle/ANIMA/3157

Introduction: Obesity is a public health problem that has reached epidemic proportions in the world. Seeks to complement the studies to clarify aspects of the pathophysiology of obesity recognizing their involvement in the impairment of cognitive functions. To evaluate inflammatory and oxidative stress parameters hippocampus, striatum and prefrontal cortex of mice subjected to obesity induced by high fat diet in order to assess the impact of obesity on cognition related structures. Methods: Swiss male mice aged 40 days, were divided into two matched groups, that received the high-fat diet control group (normolipídica diet) were subjected to 10 weeks of experiment. It was estimated body weight, visceral fat, cytokines (IL-1β, IL-10, TNF-α), oxidative damage levels in lipid and protein carbonylation and activity of superoxide dismutase and catalase in the hippocampus, striatum and prefrontal cortex. Results: In this study we identified increase in IL-1β levels in the hippocampus, striatum and prefrontal and TNF-α levels only in the striatum and hippocampus of animals when compared to the control. As the striatum there was an increase in IL-10 levels. In parameters of oxidative stress, the assessment of damage to lipids showed an increase in the hippocampus of obese animals and carbonylation proteins present in the hippocampus and striatum of obese animals. SOD activity did not occur difference and catalase activity was observed increase in prefrontal and inhibiting its activity in the hippocampus. Conclusion: We suggest that the central inflammation when installed in the hippocampus, cortex and striatum may contribute to obesity-related cognitive impairment.