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炎症小体:在创伤性脑和脊髓损伤中的作用。

Inflammasome: Its role in traumatic brain and spinal cord injury.

机构信息

Department of Anatomy, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran.

Department of Anatomy, School of Medicine, Tehran University of Medical Science, Tehran, Iran.

出版信息

J Cell Physiol. 2018 Jul;233(7):5160-5169. doi: 10.1002/jcp.26287. Epub 2018 Jan 19.

Abstract

Traumatic brain injury (TBI) and spinal cord injury (SCI) are pathological events that lead to neuropathological conditions which have in consequence the initiation of pro-inflammatory cytokine production. Neuroinflammation plays a key role in the secondary phase of both TBI and SCI after initial cell death. Activation of cytoplasmic inflammasome complexes is regarded as the essential step of neuroinflammation and a key trigger for neuronal death called pyroptosis. Inflammasome complexes are involved in activation of caspase-1 which catalyzes the cleavage of pro-interleukins into their active forms (including interleukin-18 [IL-18] and IL-1β). The focus of this article is to discuss the time-course and regulation of inflammasome assembly and activation during TBI and SCI and their targeting in designing therapeutic approaches. We particularly focus on the inflammasomes NLRP1 and NLRP3 which play a pivotal function during TBI and SCI in the central nervous system (CNS).

摘要

创伤性脑损伤(TBI)和脊髓损伤(SCI)是导致神经病理学状况的病理性事件,继而引发促炎细胞因子的产生。神经炎症在 TBI 和 SCI 的初始细胞死亡后的继发性阶段中起着关键作用。细胞质炎性小体复合物的激活被认为是神经炎症的必要步骤,也是一种称为细胞焦亡的神经元死亡的关键触发因素。炎性小体复合物参与半胱天冬酶-1 的激活,该酶催化前白细胞介素转化为其活性形式(包括白细胞介素-18 [IL-18]和白细胞介素-1β)。本文的重点是讨论 TBI 和 SCI 期间炎性小体组装和激活的时程和调节,以及针对它们设计治疗方法。我们特别关注在中枢神经系统(CNS)中,NLRP1 和 NLRP3 炎性小体在 TBI 和 SCI 中发挥关键作用。

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