中国现代神经疾病杂志 ›› 2025, Vol. 25 ›› Issue (5): 367-374. doi: 10.3969/j.issn.1672-6731.2025.05.002

• 专题综述 • 上一篇    下一篇

2 新型血液炎症标志物与缺血性卒中出血性转化关系研究进展

黄云秀1, 王亚楠2, 刘东3, 吴波1, 刘峻峰1,*()   

  1. 1. 610041 成都, 四川大学华西医院神经内科
    2. 610041 成都, 脑血管病中心
    3. 618000 四川省德阳市第二人民医院神经内科
  • 收稿日期:2025-03-30 出版日期:2025-05-25 发布日期:2025-06-05
  • 通讯作者: 刘峻峰
  • 作者简介:

    黄云秀与王亚楠对本文有同等贡献

    HUANG Yun-xiu and WANG Ya-nan contributed equally to the article

  • 基金资助:
    国家自然科学基金资助项目(82371323); 四川大学华西医院专职博士后研发基金资助项目(24HXBH139); 2023年四川省德阳市社会发展领域重点研发指导类项目(2023SZZ037)

Research progress on the relationship between novel blood inflammatory markers and hemorrhagic transformation after ischemic stroke

Yun-xiu HUANG1, Ya-nan WANG2, Dong LIU3, Bo WU1, Jun-feng LIU1,*()   

  1. 1. Department of Neurology, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, China
    2. Center of Cerebrovascular Diseases, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, China
    3. Department of Neurology, The Second People's Hospital of Deyang, Deyang 618000, Sichuan, China
  • Received:2025-03-30 Online:2025-05-25 Published:2025-06-05
  • Contact: Jun-feng LIU
  • Supported by:
    the National Natural Science Foundation of China(82371323); Postdoctor Research Fund of West China Hospital, Sichuan University(24HXBH139); 2023 Key Research and Development Guidance Project in the Field of Social Development of Deyang in Sichuan(2023SZZ037)

摘要:

出血性转化是缺血性卒中的自然病程或静脉溶栓、机械取栓等治疗的严重并发症之一,增加患者不良预后风险,影响临床治疗决策。血脑屏障损伤是出血性转化的核心机制,炎症反应通过激活内皮细胞、招募中性粒细胞和巨噬细胞等免疫细胞,释放蛋白酶、活性氧等炎性介质,加剧血管损伤和血脑屏障损伤,促进出血性转化。血液炎症标志物可反映这一病理改变过程,为出血性转化的早期识别和风险分层提供重要信息。经典炎症标志物如基质金属蛋白酶⁃9、铁蛋白等已被证实可用于预测出血性转化,中性粒细胞明胶酶相关脂质运载蛋白、高迁移率族蛋白B1和核苷酸结合寡聚化结构域样受体蛋白3炎症小体等新型标志物在出血性转化中的作用机制及预测潜力逐渐成为研究热点。本文聚焦新型血液炎症标志物,阐述其与出血性转化的临床关联及研究进展,旨在为出血性转化的机制解析、精准预测及个性化治疗提供依据。

关键词: 缺血性卒中, 脑出血, 炎症, 生物标记, 血液, 综述

Abstract:

Hemorrhagic transformation (HT) is one of the severe complications of ischemic stroke, which may occur either during the natural course or as a consequence of treatments such as thrombolysis and thrombectomy. HT is associated with poor prognosis after ischemic stroke and influences clinical treatment decisions. Disruption of blood-brain barrier (BBB) has been demonstrated as the main mechanism underlying HT. Inflammatory responses contribute to this process by activating endothelial cells, recruiting immune cells such as neutrophils and macrophages, and releasing inflammatory mediators including proteases and reactive oxygen species, which further exacerbate vascular injury and BBB permeability, thereby promoting HT. Blood inflammatory markers may reflect these pathological processes and offer valuable biological information for early identification and risk stratification of HT. Classical inflammatory markers, such as matrix metalloproteinase-9 (MMP-9) and ferritin, have been demonstrated predictive value for HT. Recently increasing attention has been paid to investigate the mechanism and predictive potential of novel markers, such as neutrophil gelatinase-associated lipocalin (NGAL), high-mobility group box 1 (HMGB1) and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, for predicting HT. This review focuses on the novel blood inflammatory markers and systematically describes their correlation with HT, with the aim of providing a scientific basis for the mechanism investigation, accurate prediction and individualized therapeutic strategies of HT.

Key words: Ischemic stroke, Cerebral hemorrhage, Inflammation, Biomarkers, Blood, Review