Post-traumatic stress disorder (PTSD) is a chronic incapacitating condition with recurrent experience of trauma-related memories, negative mood, altered cognition, and hypervigilance. Agglomeration of preclinical and clinical evidence in recent years specified that alterations in neural networks favor certain characteristics of PTSD. Besides the disruption of hypothalamus-pituitary-axis (HPA) axis, intensified immune status with elevated pro-inflammatory cytokines and arachidonic metabolites of COX-2 such as PGE2 creates a putative scenario in worsening the neurobehavioral facet of PTSD. This review aims to link the Diagnostic and Statistical Manual of mental disorders (DSM-V) symptomology to major neural mechanisms that are supposed to underpin the transition from acute stress reactions to the development of PTSD. Also, to demonstrate how these intertwined processes can be applied to probable early intervention strategies followed by a description of the evidence supporting the proposed mechanisms. Hence in this review, several neural network mechanisms were postulated concerning the HPA axis, COX-2, PGE2, NLRP3, and sirtuins to unravel possible complex neuroinflammatory mechanisms that are obscured in PTSD condition.

创伤后应激障碍 (PTSD) 是一种慢性失能疾病，反复出现与创伤相关的记忆、消极情绪、认知改变和过度警觉。近年来的临床前和临床证据表明，神经网络的改变有利于 PTSD 的某些特征。除了下丘脑-垂体轴 (HPA) 轴的破坏之外，促炎细胞因子和 COX-2 花生四烯酸代谢物（如 PGE2）升高导致的免疫状态增强，也造成了 PTSD 神经行为方面恶化的假定情况。本综述旨在将《精神障碍诊断与统计手册》(DSM-V) 症状学与主要神经机制联系起来，这些机制被认为支持从急性应激反应到 PTSD 发展的转变。此外，为了演示如何将这些相互交织的过程应用于可能的早期干预策略，然后描述支持拟议机制的证据。因此，在这篇综述中，假设了几种与 HPA 轴、COX-2、PGE2、NLRP3 和 Sirtuins 相关的神经网络机制，以阐明在 PTSD 条件下可能被掩盖的复杂神经炎症机制。