中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (1): 62-80.doi: 10.4103/NRR.NRR-D-24-00917

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

NLRP3炎症小体与微生物-肠道-大脑轴：脑内出血后白质损伤的新视角

  

  • 出版日期:2026-01-15 发布日期:2025-04-18
  • 基金资助:
    本研究得到广东省基础与应用基础研究基金[2023A1515030045]和南方医科大学珠江医院院长基金[yzjj2022ms4]的资助。 南方医科大学珠江医院院长基金，编号：[yzjj2022ms4]。

NLRP3 inflammasome and gut microbiota–brain axis: A new perspective on white matter injury after intracerebral hemorrhage

Xiaoxi Cai1, 2, #, Xinhong Cai1, 2, #, Quanhua Xie1, 2, #, Xueqi Xiao1, 2, Tong Li1, 2, Tian Zhou3, *, Haitao Sun1, 2, 3, *   

  1. 1 Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, The Second School of Clinical Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China;  2 Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China;  3 Key Laboratory of Mental Health of the Ministry of Education, Guangdong–Hong Kong–Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Southern Medical University, Guangzhou, Guangdong Province, China
  • Online:2026-01-15 Published:2025-04-18
  • Contact: Haitao Sun, PhD, MD, 2009sht@smu.edu.cn; Tian Zhou, MD, tianzhou_tz@163.com
  • Supported by:
    This work was supported by the Guangdong Basic and Applied Basic Research Foundation, No. 2023A1515030045 (to HS); Presidential Foundation of Zhujiang Hospital of Southern Medical University, No. yzjj2022ms4 (to HS).

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摘要：

脑出血是脑卒中中最危险的亚型，具有高死亡率和发病率，且常导致严重的继发性白质损伤。近几十年来，研究发现肠道微生物群可以通过微生物群-肠道-脑轴与大脑进行双向交流。通过微生物群-肠道-脑轴，肠道微生物群与脑出血及其继发性白质损伤的发展和预后密切相关，其中NLRP3炎症小体在其中占据重要地位。文章综述了脑出血后体内肠道微生物群的失调，以及这种失衡促进NLRP3炎症小体激活的可能机制，如代谢途径（短链脂肪酸、脂多糖、乳酸、胆汁酸、三甲胺-N-氧化物、色氨酸）、神经途径（迷走神经、交感神经）和免疫途径（小胶质细胞、T细胞）。文章还讨论了激活的NLRP3炎症小体与脑出血后继发性白质损伤之间的关系。激活的NLRP3炎症小体可通过促进血脑屏障的破坏、诱导神经炎症和干扰神经再生来加重脑出血后的继发性白质损伤。最后，文章介绍了脑出血及其继发性白质损伤的治疗策略。总之，文章揭示了微生物群-肠道-脑轴和NLRP3在脑出血后白质损伤中的关键作用，这将有助于进一步探索潜在的治疗方法。

https://orcid.org/0000-0001-7925-9506 (Haitao Sun); https://orcid.org/0000-0002-4981-7981 (Tian Zhou)

关键词: 肠道微生物群, 免疫, 脑内出血, 微生物群-肠道-脑轴, 神经炎症, NLRP3蛋白, 白质损伤, 脑卒中, 治疗学

Abstract: Intracerebral hemorrhage is the most dangerous subtype of stroke, characterized by high mortality and morbidity rates, and frequently leads to significant secondary white matter injury. In recent decades, studies have revealed that gut microbiota can communicate bidirectionally with the brain through the gut microbiota–brain axis. This axis indicates that gut microbiota is closely related to the development and prognosis of intracerebral hemorrhage and its associated secondary white matter injury. The NACHT, LRR, and pyrin domain-containing protein 3 (NLRP3) inflammasome plays a crucial role in this context. This review summarizes the dysbiosis of gut microbiota following intracerebral hemorrhage and explores the mechanisms by which this imbalance may promote the activation of the NLRP3 inflammasome. These mechanisms include metabolic pathways (involving short-chain fatty acids, lipopolysaccharides, lactic acid, bile acids, trimethylamine-N-oxide, and tryptophan), neural pathways (such as the vagus nerve and sympathetic nerve), and immune pathways (involving microglia and T cells). We then discuss the relationship between the activated NLRP3 inflammasome and secondary white matter injury after intracerebral hemorrhage. The activation of the NLRP3 inflammasome can exacerbate secondary white matter injury by disrupting the blood–brain barrier, inducing neuroinflammation, and interfering with nerve regeneration. Finally, we outline potential treatment strategies for intracerebral hemorrhage and its secondary white matter injury. Our review highlights the critical role of the gut microbiota–brain axis and the NLRP3 inflammasome in white matter injury following intracerebral hemorrhage, paving the way for exploring potential therapeutic approaches.

Key words: gut microbiota, gut microbiota–brain axis, immune, intracerebral hemorrhage, neuroinflammation, NLRP3 protein, stroke, therapeutics, white matter injury