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