基础医学与临床 ›› 2026, Vol. 46 ›› Issue (3): 435-439.doi: 10.16352/j.issn.1001-6325.2026.03.0435

• 短篇综述 • 上一篇    下一篇

治疗脑缺血/再灌注损伤中NLRP3炎性小体介导的细胞焦亡的研究进展

杨溢伟1, 孙晓伟2*   

  1. 1.黑龙江中医药大学 第一临床医学院,黑龙江 哈尔滨 150040;
    2.黑龙江中医药大学附属第一医院 康复二科,黑龙江 哈尔滨 150040
  • 收稿日期:2025-06-03 修回日期:2025-09-24 出版日期:2026-03-05 发布日期:2026-02-25
  • 通讯作者: *gemini19790530@163.com
  • 基金资助:
    黑龙江省自然科学基金(LH2024H051)

Research progress in the treatment of NLRP3 inflammasome-mediated pyroptosis in cerebral ischemia-reperfusion injury

YANG Yiwei1, SUN Xiaowei2*   

  1. 1. The First Clinical College of Heilongjiang University of Chinese Medicine, Harbin 150040;
    2. Department of Rehabilitation 2, the First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150040, China
  • Received:2025-06-03 Revised:2025-09-24 Online:2026-03-05 Published:2026-02-25
  • Contact: *gemini19790530@163.com

摘要: 脑缺血/再灌注损伤(CI/RI)是缺血性卒中后神经功能恶化的重要原因,其机制与NLRP3炎性小体介导的细胞焦亡有关。NLRP3炎性小体受多种病理机制的影响被激活,促进caspase-1依赖的gasdermin D裂解,引发细胞膜孔道形成及炎性因子(IL-1β、IL-18)释放,从而导致细胞焦亡的发生,细胞焦亡作为一种具有明显炎性反应特征的细胞死亡方式,会造成并加剧神经炎性反应。

关键词: NOD样受体热蛋白结构域相关蛋白3(NLRP3), 细胞焦亡, 脑缺血/再灌注损伤

Abstract: Cerebral ischemia-reperfusion injury (CI/RI) is an important cause of neurological deterioration after ischemic stroke, and its mechanism is related to pyroptosis mediated by NLRP3 inflammasomes. The NLRP3 inflammasome is activated under the influence of multiple pathological mechanisms, promoting caspase-1-dependent gasdermin D lyses, triggering the formation of cell membrane pores and the release of inflammatory factors (IL-1β, IL-18), thereby leading to the occurrence of pyroptosis. Pyroptosis, as a type of cell death with obvious inflammatory response characteristics, It will cause and exacerbate neuroinflammatory responses.

Key words: NOD-, LRR-and pyrin domain-containing protein 3(NLRP3), pyroptosis, cerebral ischemia-reperfusion injury

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