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- Viviane Nogueira de Zorzi, Fernanda Haupenthal, Alexandra Seide Cardoso, Gustavo Cassol, Valdir A Facundo, Laudir J Bálico, Daniella K S Lima, Santos Adair Roberto Soares ARS Laboratório de Neurobiologia da Dor e Inflamação, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC, Ana Flavia Furian, Mauro Schneider Oliveira, Royes Luiz Fernando Freire LFF Laboratório de Bioquímica do Exercício, Centro de Educação Física e Desportos, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil, and Michele Rechia Fighera.
- Departamento de Neuropsiquiatria, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil; Laboratório de Bioquímica do Exercício, Centro de Educação Física e Desportos, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil; Programa de Pós-graduação em Ciências Biológicas, Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
- Neuroscience. 2019 Aug 10; 413: 154-168.
AbstractEpilepsy is one of the most common chronic neurological diseases. It is characterized by recurrent epileptic seizures, where one-third of patients are refractory to existing treatments. Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there is a pronounced increase in the expression of key inflammatory mediators, such as prostaglandin E2 (PGE2), during seizures. The purpose of this study was to investigate whether PGE2 increases susceptibility to pentylenetetrazol-induced (PTZ) seizures. Subsequently, we evaluated if the flavonoid isolated from the plant Piper aleyreanum (galangin) presented any anticonvulsive effects. Our results demonstrated that the group treated with PGE2 increased susceptibility to PTZ and caused myoclonic and generalized seizures, which increased seizure duration and electroencephalographic wave amplitudes. Furthermore, treatment with PGE2 and PTZ increased IBA-1 (microglial marker), GFAP (astrocytic marker), 4-HNE (lipid peroxidation marker), VCAM-1 (vascular cell adhesion molecule 1), and p-PKAIIα (phosphorylated cAMP-dependent protein kinase) immunocontent. Indeed, galangin prevented behavioral and electroencephalographic seizures, reactive species production, decreased microglial and astrocytic immunocontent, as well as decreased VCAM-1 immunocontent and p-PKA/PKA ratio induced by PGE2/PTZ. Therefore, this study suggests galangin may have an antagonizing role on PGE2-induced effects, reducing cerebral inflammation and protecting from excitatory effects evidenced by administrating PGE2 and PTZ. However, further studies are needed to investigate the clinical implications of the findings and their underlying mechanisms.Copyright © 2019. Published by Elsevier Ltd.
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