Microdose Lithium Treatment Reduced Inflammatory Factors and Neurodegeneration in Organotypic Hippocampal Culture of Old SAMP-8 Mice

Autor(es)

Toricelli, Mariana ^[1] ; Evangelista, Sebastiana Ribeiro ^[1] ; Buck, Hudson Sousa ^[1] ; Viel, Tania Araujo ^[2]

Afiliação do(s) autor(es)

^[1] Santa Casa Sao Paulo Sch Med Sci, Dept Physiol Sci, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Sch Arts Sci & Humanities, Lab Neuropharmacol Aging, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Cellular and Molecular Neurobiology; v. 41, n. 7, p. 1509-1520, OCT 2021.
• Citações Web of Science: 2

Resumo

It was already shown that microdoses of lithium carbonate (Li2CO3) promoted memory stabilization in humans and mice. Prolonged treatment also reduced neuronal loss and increased the density of the neurotrophin BDNF in transgenic mice for Alzheimer's disease. The aim of this study was to evaluate whether lithium ions affect inflammatory profiles and neuronal integrity in an animal model of accelerated senescence (SAMP-8). Organotypic hippocampal cultures obtained from 11 to 12-month-old SAMP-8 mice were treated with 2 mu M, 20 mu M and 200 mu M Li2CO3. 2 mu M Li(2)CO(3)promoted a significant reduction in propidium iodide uptake in the CA2 area of hippocampus, whereas 20 mu M promoted neuroprotection in the CA3 and GrDG areas. 200 mu M caused an increase in cellular death, showing toxicity. Measured with quantitative PCR, IL-1 alpha, IL-6 and MIP-1B/CCL-4 gene expression was significantly reduced with 20 mu M Li2CO3, whereas IL-10 gene expression was significantly increased with the same concentration. In addition, 2 mu M and 20 mu M Li(2)CO(3)were also effective in reducing the activation of NFkB and inflammatory cytokines densities, as evaluated by ELISA. It is concluded that very low doses of Li(2)CO(3)can play an important role in neuroprotection as it can reduce neuronal loss and neuroinflammation in older individuals. (AU)

• Processo FAPESP: 16/07115-6 - Estudo translacional de estratégias e biomarcadores para a promoção da longevidade saudável
• Beneficiário: Tânia Araújo Viel
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 17/21655-6 - Estudo da modulação de vias de sobrevivência celular pelo receptor B2 da bradicinina e seu impacto na neuroinflamação, em cultura organotípica de hipocampo de camundongo transgênico para a doença de Alzheimer
• Beneficiário: Mariana Toricelli Pinto
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado