Department of Rehabilitation, The First Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Department of General Medicine, Jiangkou Town Center Hospital, Ganxian 341100, China.
Int Immunopharmacol. 2023 Apr;117:109926. doi: 10.1016/j.intimp.2023.109926. Epub 2023 Mar 11.
Interleukin-17A (IL-17A) plays an important role in the progression of ischemic stroke. IL-17A mediates the endothelial inflammatory response, promotes water and sodium retention, and changes the electrophysiological structure of the atrium, accelerating the progression of ischemic stroke risk factors such as atherosclerotic plaques, hypertension, and atrial fibrillation. In the acute phase of ischemic stroke, IL-17A mediates neuronal injury through neutrophil chemotaxis to the site of injury, the induction of neuronal apoptosis, and activation of the calpain-TRPC-6 (transient receptor potential channel-6) pathway. During ischemic stroke recovery, IL-17A, which is mainly derived from reactive astrocytes, promotes and maintains the survival of neural precursor cells (NPCs) in the subventricular zone (SVZ), neuronal differentiation, and synapse formation and participates in the repair of neurological function. Therapies targeting IL-17A-associated inflammatory signaling pathways can reduce the risk of ischemic stroke and neuronal damage and are a new therapeutic strategy for ischemic stroke and its risk factors. In this paper, we will briefly discuss the pathophysiological role of IL-17A in ischemic stroke risk factors, acute and chronic inflammatory responses, and the potential therapeutic value of targeting IL-17A.
白细胞介素-17A（IL-17A）在缺血性中风的进展中起着重要作用。IL-17A 介导内皮炎症反应，促进水钠潴留，并改变心房的电生理结构，加速动脉粥样硬化斑块、高血压和心房颤动等缺血性中风危险因素的进展。在缺血性中风的急性期，IL-17A 通过中性粒细胞向损伤部位趋化、诱导神经元凋亡和激活钙蛋白酶-TRPC-6（瞬时受体电位通道-6）途径来介导神经元损伤。在缺血性中风恢复期间，主要来源于反应性星形胶质细胞的 IL-17A 促进和维持侧脑室下区（SVZ）中的神经前体细胞（NPC）的存活、神经元分化以及突触形成，并参与神经功能的修复。针对与 IL-17A 相关的炎症信号通路的治疗方法可以降低缺血性中风和神经元损伤的风险，是缺血性中风及其危险因素的一种新的治疗策略。本文将简要讨论 IL-17A 在缺血性中风危险因素、急性和慢性炎症反应中的病理生理作用，以及靶向 IL-17A 的潜在治疗价值。
