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系统凝血酶抑制可改善匹鲁卡品诱导癫痫持续状态小鼠模型的癫痫发作。

Systemic thrombin inhibition ameliorates seizures in a mouse model of pilocarpine-induced status epilepticus.

机构信息

Department of Neuroanatomy, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.

Department of Neurology, The Chaim Sheba Medical Center, Tel HaShomer, Israel.

出版信息

J Mol Med (Berl). 2019 Nov;97(11):1567-1574. doi: 10.1007/s00109-019-01837-2. Epub 2019 Oct 31.

Abstract

Status epilepticus (SE) is a life-threatening condition characterized by ongoing seizure activity which can lead to severe brain damage and death if not treated properly. Recent work suggests that alterations in blood-brain barrier (BBB) function and subsequent cortical exposure to coagulation factors may initiate, promote, and/or sustain SE. This suggestion is based on the observation that the serine protease thrombin, which plays a fundamental role in the blood coagulation cascade, increases neural excitability through the activation of protease-activated receptor 1 (PAR1). However, it remains unclear whether systemic inhibition of thrombin asserts "anti-epileptic" effects in vivo. We here used the pilocarpine model of SE in adult 3-month-old male mice to address the question whether intraperitoneal injection of the thrombin inhibitor α-NAPAP (0.75 mg/kg) counters SE. Indeed, pharmacological inhibition of thrombin ameliorates the behavioral outcome of pilocarpine-induced SE. Similar results are obtained when the thrombin receptor PAR1 is pharmacologically blocked using intraperitoneal injection of SCH79797 (25 μg/kg) prior to SE induction. Consistent with these results, an increase in thrombin immunofluorescence is detected in the hippocampus of pilocarpine-treated animals. Moreover, increased hippocampal serine protease activity is detected 90 min after SE induction, which is not observed in animals treated with α-NAPAP prior to SE induction. Together, these results corroborate and extend recent studies suggesting that novel oral anticoagulants which target thrombin (and PAR1) may assert anti-epileptic effects in vivo. KEY MESSAGES: Systemic thrombin/PAR1-inhibition ameliorates anticoagulants behavioral seizures. Status epilepticus increases thrombin levels in the hippocampus. Increased serine protease activity in the hippocampus after status epileptic. Anti-epileptic potential of clinically used anticoagulants must be evaluated.

摘要

癫痫持续状态(SE)是一种危及生命的疾病,其特征是持续的癫痫发作,如果得不到适当的治疗,可能会导致严重的脑损伤和死亡。最近的研究表明,血脑屏障(BBB)功能的改变以及随后皮质暴露于凝血因子可能启动、促进和/或维持 SE。这一观点是基于这样的观察结果,即丝氨酸蛋白酶凝血酶在凝血级联反应中起着至关重要的作用,通过激活蛋白酶激活受体 1(PAR1)增加神经兴奋性。然而,目前尚不清楚全身抑制凝血酶是否在体内具有“抗癫痫”作用。我们在这里使用成年 3 个月大雄性小鼠的匹罗卡品 SE 模型来解决以下问题:腹腔注射凝血酶抑制剂 α-NAPAP(0.75mg/kg)是否能对抗 SE。事实上,凝血酶的药理学抑制可改善匹罗卡品诱导的 SE 的行为结果。当在 SE 诱导前通过腹腔注射 SCH79797(25μg/kg)药理学阻断凝血酶受体 PAR1 时,也会得到类似的结果。与这些结果一致的是,在匹罗卡品处理的动物的海马体中检测到凝血酶免疫荧光增加。此外,在 SE 诱导后 90 分钟检测到海马丝氨酸蛋白酶活性增加,而在 SE 诱导前用 α-NAPAP 处理的动物中未观察到这种情况。综上所述,这些结果证实并扩展了最近的研究,表明针对凝血酶(和 PAR1)的新型口服抗凝剂可能在体内具有抗癫痫作用。 关键信息:全身凝血酶/PAR1 抑制可改善抗凝剂引起的癫痫发作。癫痫持续状态增加海马体中的凝血酶水平。癫痫持续状态后海马体中丝氨酸蛋白酶活性增加。必须评估临床使用的抗凝剂的抗癫痫潜力。

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