Department of Neurology, the First Affiliated Hospital of Soochow University, Suzhou, 215000, China.
Department of Neurology, Suzhou Yongding Hospital, Suzhou, 215028, China.
Mol Neurobiol. 2024 Jan;61(1):132-147. doi: 10.1007/s12035-023-03563-w. Epub 2023 Aug 17.
Post-stroke depression (PSD) affects approximately one-third of stroke survivors, severely impacting general recovery and quality of life. Despite extensive studies, the exact mechanisms underlying PSD remain elusive. However, emerging evidence implicates proinflammatory cytokines, including interleukin-1β, interleukin-6, tumor necrosis factor-alpha, and interleukin-18, play critical roles in PSD development. These cytokines contribute to PSD through various mechanisms, including hypothalamic-pituitary-adrenal (HPA) axis dysfunction, neurotransmitter alterations, neurotrophic factor changes, gut microbiota imbalances, and genetic predispositions. This review is aimed at exploring the role of cytokines in stroke and PSD while identifying their potential as specific therapeutic targets for managing PSD. A more profound understanding of the mechanisms regulating inflammatory cytokine expression and anti-inflammatory cytokines like interleukin-10 in PSD may facilitate the development of innovative interventions to improve outcomes for stroke survivors experiencing depression.
脑卒中后抑郁(PSD)影响约三分之一的脑卒中幸存者,严重影响整体康复和生活质量。尽管进行了广泛的研究,但 PSD 的确切机制仍难以捉摸。然而,新出现的证据表明,促炎细胞因子,包括白细胞介素-1β、白细胞介素-6、肿瘤坏死因子-α和白细胞介素-18,在 PSD 的发展中起关键作用。这些细胞因子通过多种机制导致 PSD,包括下丘脑-垂体-肾上腺(HPA)轴功能障碍、神经递质改变、神经营养因子变化、肠道微生物群失衡和遗传易感性。本综述旨在探讨细胞因子在脑卒中及其 PSD 中的作用,同时确定它们作为管理 PSD 的特定治疗靶点的潜力。更深入地了解调节 PSD 中炎症细胞因子表达和抗炎细胞因子(如白细胞介素-10)的机制,可能有助于开发创新干预措施,改善经历抑郁的脑卒中幸存者的结局。