Departamento de Neurologia e Neurocirurgia da Universidade Federal de São Paulo (UNIFESP), Sao Paulo, Brazil.
Epilepsy Behav. 2011 Jan;20(1):1-5. doi: 10.1016/j.yebeh.2010.10.001. Epub 2010 Dec 3.
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.
他汀类药物可能通过抑制炎症反应、减少氧化应激以及降低脑缺血性损伤后的体温来发挥作用。先前的数据表明，他汀类药物可保护神经元免受长时间癫痫持续状态（SE）的死亡，并减轻用海人酸处理的动物的癫痫发作行为。在这种情况下，这里描述的研究旨在研究洛伐他汀对体温和海马细胞因子（如白细胞介素-1β、白细胞介素-6、肿瘤坏死因子α以及缓激肽 B1 和 B2 受体）mRNA 表达水平的影响，这些细胞因子在匹罗卡品诱导的 SE 大鼠中。实时定量聚合酶链反应显示，与未经 SE 处理的大鼠相比，用洛伐他汀治疗 SE 的大鼠的白细胞介素-1β、白细胞介素-6、肿瘤坏死因子α和缓激肽 B1 受体的 mRNA 表达显著降低（P<0.001）。洛伐他汀还降低了 SE 诱导的发热，表明在与急性兴奋毒性或长时间 SE 相关的条件下，这种药物会引发与脑保护相关的机制。
