Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/33295
Title: Lovastatin decreases the synthesis of inflammatory mediators in the hippocampus and blocks the hyperthermia of rats submitted to long-lasting status epilepticus
Authors: Furtado Gouveia, Telma Luciana [UNIFESP]
Scorza, Fulvio Alexandre [UNIFESP]
Vieira Silva, Michele Juliana [UNIFESP]
Bandeira, Tatiane de Aquino [UNIFESP]
Perosa, Sandra Regina [UNIFESP]
Arganaraz, Gustavo Adolfo [UNIFESP]
Silva, Marcelo de Paula [UNIFESP]
Araujo, Thiago Rodrigues [UNIFESP]
Berzaghi Frangiotti, Maria Isabel [UNIFESP]
Amado, Debora [UNIFESP]
Cavalheiro, Esper Abrao [UNIFESP]
Silva, Jose Antonio
Naffah-Mazzacoratti, Maria da Graca [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Univ Nove Julho
Univ Fed Rio Grande do Norte
Keywords: Lovastatin
Inflammatory mediators
Hippocampus
Temporal lobe epilepsy
Neuroprotection
Issue Date: 1-Jan-2011
Publisher: Elsevier B.V.
Citation: Epilepsy & Behavior. San Diego: Academic Press Inc Elsevier Science, v. 20, n. 1, p. 1-5, 2011.
Abstract: Statins may act on inflammatory responses, decreasing oxidative stress and also reducing temperature after a brain ischemic insult. Previous data have indicated that statins protect neurons from death during long-lasting status epilepticus (SE) and attenuate seizure behaviors in animals treated with kainic acid. in this context, the study described here aimed to investigate the effect of lovastatin on body temperature and on mRNA expression levels of hippocampal cytokines such as interleukin-1 beta, interleukin-6, tumor necrosis factor a, and kinin B1 and B2 receptors of rats submitted to pilocarpine-induced SE. Quantitative real-time polymerase chain reaction showed a significant decrease in mRNA expression of interleukin-1 beta, interleukin-6, tumor necrosis factor a, and kinin B1 receptor in animals with SE treated with lovastatin, compared with untreated animals with SE (P<0.001). Lovastatin also reduced SE-induced hyperthermia, indicating that mechanisms related to brain protection are triggered by this drug under conditions associated with acute excitotoxicity or long-lasting SE. (c) 2010 Elsevier Inc. All rights reserved.
URI: http://repositorio.unifesp.br/handle/11600/33295
ISSN: 1525-5050
Other Identifiers: http://dx.doi.org/10.1016/j.yebeh.2010.10.001
Appears in Collections:Em verificação - Geral

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