Lovastatin decreases the synthesis of inflammatory mediators in the hippocampus and blocks the hyperthermia of rats submitted to long-lasting status epilepticus

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• 作者：Telma Luciana Furtado Gouveia^a ; Fulvio Alexandre Scorza^a ; Michele Juliana Vieira Silva^a ; Tatiane de Aquino Bandeira^a ; Sandra Regina Perosa^a ; Gustavo Adolfo Argañ ; araz^a ; ^d ; Marcelo de Paula Silva^a ; Thiago Rodrigues Araujo^a ; Maria Isabel Berzaghi Frangiotti^a ; Dé ; bora Amado^a ; Esper Abr&#xe3 ; o Cavalheiro^a ; José ; Antonio Silva Jr.^b ; Maria da Graç ; a Naffah-Mazzacoratti^c ; ^{naffahmazz.nexp@epm.br}
• 关键词：Lovastatin ; Inflammatory mediators ; Hippocampus ; Temporal lobe epilepsy ; Neuroprotection
• 刊名：Epilepsy & Behavior
• 出版年：2011
• 出版时间：January 2011
• 年：2011
• 卷：20
• 期：1
• 页码：1-5
• 全文大小：371 K

文摘

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-1β, interleukin-6, tumor necrosis factor α, 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-1β, interleukin-6, tumor necrosis factor α, 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.