| Texto completo | |
| Autor(es): Mostrar menos - |
Pinz, Mikaela Peglow
;
de Oliveira, Renata Leivas
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Ramson da Fonseca, Caren Aline
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Voss, Guilherme Teixeira
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da Silva, Beatriz Pereira
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Barbosa Duarte, Luis Fernando
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Domingues, William Borges
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Ortiz, Hadassa Gabriela
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Pinto Savall, Anne Suely
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Meotti, Flavia Carla
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Alves, Diego
;
Campos, Vinicius Farias
;
Pinton, Simone
;
Wilhelm, Ethel Antunes
;
Luchese, Cristiane
Número total de Autores: 15
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| Tipo de documento: | Artigo Científico |
| Fonte: | Molecular Neurobiology; v. N/A, p. 18-pg., 2022-11-24. |
| Resumo | |
In the present study, the effect of 6-((4-fluorophenyl) selanyl)-9H-purine (FSP) was tested against memory impairment and sensitivity to nociception induced by intracerebroventricular injection of amyloid-beta peptide (A beta) (25-35 fragment), 3 nmol/3 mu l/per site in mice. Memory impairment was determined by the object recognition task (ORT) and nociception by the Von-Frey test (VFT). A beta caused neuroinflammation with upregulation of glial fibrillary acidic protein (GFAP) (in hippocampus), nuclear factor-kappa B (NF-kappa B), and the proinflammatory cytokines interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in cerebral cortex and hippocampus. Additionally, A beta increased oxidant levels and lipid peroxidation in cerebral cortex and hippocampus, but decreased heme oxygenase-1 (HO-1) and peroxiredoxin-1 (Prdx1) expression in the hippocampus. Anti-neuroinflammatory effects of FSP were demonstrated by a decrease in the expression of GFAP and NF-kappa B in the hippocampus, as well as a decrease in proinflammatory cytokines in both the hippocampus and cerebral cortex FSP protected against oxidative stress by decreasing oxidant levels and lipid peroxidation and by increasing HO-1 and Prdx1 expressions in the hippocampus of mice. Moreover, FSP prevented the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2) in the hippocampus of mice induced by A beta. In conclusion, treatment with FSP attenuated memory impairment, nociception sensitivity by decreasing oxidative stress, and neuroinflammation in a mouse model of Alzheimer's disease. (AU) | |
| Processo FAPESP: | 13/07937-8 - Redoxoma |
| Beneficiário: | Ohara Augusto |
| Modalidade de apoio: | Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs |
| Processo FAPESP: | 18/14898-2 - Processos redox na inflamação e o seu papel sobre doenças inflamatórias |
| Beneficiário: | Flavia Carla Meotti |
| Modalidade de apoio: | Auxílio à Pesquisa - Jovens Pesquisadores - Fase 2 |