Efeitos do dimetilsulfóxido (DMSO) sobre os prejuízos de memória induzidos pela estreptozotocina em ratos Wistar

• Ano de defesa: 2019
• Autor(a) principal: Clímaco, Valter Malaguido
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Positivo; Brasil; Pós-Graduação; Programa de Pós-Graduação em Biotecnologia Industrial; UP
• Palavras-chave em Português: Dimetilsulfóxido; Estreptozotocina; Memória; Neurodegeneração; Doença de Alzheimer; Labirinto aquatico de Morris; CNPQ::CIENCIAS BIOLOGICAS::BIOLOGIA GERAL
• Link de acesso: https://repositorio.cruzeirodosul.edu.br/handle/123456789/2279

Neurodegenerative diseases, such as Alzheimer's disease, irreversibly impair cell dynamics without curative treatment. Dimethylsulfoxide (DMSO) has a wide molecular versatility, with several neurochemical and therapeutic actions not exploited. The aim of the present paper is to investigate the potential neuroprotective effect of Dimethyl sulfoxide (DMSO) on Streptozotocin (STZ) induced spatial memory impairment in rats. We used fourty-two male wistar rats divided into four groups: Control Group (icv) vehicle and intraperitoneal saline (ip) (n = 11); STZ 3mg/kg group, via icv and ip saline = 10); SZT group, icv + DMSO 0.75 g/kg to 40% diluted in saline solution 0.9% ip (n = 11); and STZ group, icv + DMSO 1.5 g / kg to 40% diluted in saline 0 , 9% ip (n = 10). It took five days of treatment starting 24 hours after vehicle or STZ administration. Also twenty-four hours after the last treatment, the animals were submitted to spatial memory tests in the Morris water maze, in which spatial memory and reference memory were evaluated. At the end of the tests, the animals were euthanized and the brains dissected bilaterally for the hippocampus removal. Molecular analyzes were performed by means of qPCR to investigate the expression profile of genes related to inflammation (interleukin 1-beta, IL-1β, tumor necrosis factor α, TNF-α), reactive species of mitochondrial oxidative stress (catalase; CAT) and activator of adult neurogenesis (brain-derived neurotrophic factor; BDNF). Behavioral results of reference and working memory, there was no significant improvement of spatial learning strategies in the treatment groups with DMSO, which included the acute injury time induced directly on the hippocampal target and a short treatment of 5 days following literature models. Molecular analyzes of expression of genes involved in neuroinflammation (IL-1β, TNF-α) and oxidative stress (CAT) did not show statistical differences between the experimental groups, however reduction trends in IL1-β, TNFα, CAT expression and BDNF elevation in the DMSO treated group, at a dose of 1,5 g/kg suggest the most favorable cellular environment at the molecular level against neurodegeneration and the facilitation of neuroprotection throught BDNF in the pathways of cellular survival, synaptic plasticity and axonal budding.