RESUMO
The primary features of Alzheimers disease (AD) are extracellular amyloid plaques consisting mainly of deposits of amyloid β (Aβ) peptides and intracellular neurofibrillary tangles (NFTs). Sets of evidence suggest that interleukin-5 (IL-5) is involved in the pathogenesis of AD. Herein, we investigated the protective role of IL-5 in PC12 cells, to provide new insights into understanding this disease. Western blot was employed to assess the protein levels of Bax and phospho-tau as well as phospho-JAK2; MTT assay was performed to decipher cell viability. Treatment of IL-5 decreased Aβ25-35-induced tau phosphorylation and apoptosis, effects blunted by JAK2 inhibition. IL-5 prevents Aβ25-35-evoked tau protein hyperphosphorylation and apoptosis through JAK2 signaling (AU)
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Assuntos
Animais , Ratos , Neurônios/metabolismo , Interleucina-5/metabolismo , Apoptose , Peptídeos beta-Amiloides/metabolismo , Subunidade alfa de Receptor de Interleucina-5/agonistas , Proteínas tau/metabolismo , Processamento de Proteína Pós-Traducional , Doença de Alzheimer , Sulfonamidas/farmacologia , Sobrevivência Celular , Ativação Enzimática , Janus Quinase 2 , Proteínas do Tecido Nervoso , Células PC12 , Pirrolidinas/farmacologia , Interferência de RNA , Inibidores de Proteínas Quinases/farmacologiaRESUMO
The primary features of Alzheimer's disease (AD) are extracellular amyloid plaques consisting mainly of deposits of amyloid ß (Aß) peptides and intracellular neurofibrillary tangles (NFTs). Sets of evidence suggest that interleukin-5 (IL-5) is involved in the pathogenesis of AD. Herein, we investigated the protective role of IL-5 in PC12 cells, to provide new insights into understanding this disease. Western blot was employed to assess the protein levels of Bax and phospho-tau as well as phospho-JAK2; MTT assay was performed to decipher cell viability. Treatment of IL-5 decreased Aß25-35-induced tau phosphorylation and apoptosis, effects blunted by JAK2 inhibition. IL-5 prevents Aß25-35-evoked tau protein hyperphosphorylation and apoptosis through JAK2 signaling.
