Influence of the brain-gut axis on neuroinflammation in cerebral ischemia-reperfusion injury (Review)

被引:2
|
作者
Zhang, Yifeng [1 ]
Yang, Hang [2 ]
Hou, Shuai [2 ]
Xia, Yulei [1 ]
Wang, Yan-Qiang [1 ]
机构
[1] Weifang Med Univ, Affiliated Hosp, Sch Clin Med, Dept Neurol 2, 2428 Yuhe Rd, Weifang 261041, Shandong, Peoples R China
[2] Weifang Med Univ, Affiliated Hosp, Sch Clin Med, Dept Emergency, Weifang 261041, Shandong, Peoples R China
关键词
GBMA; CI/RI; cGAS-STING; gut microbial metabolites; neuroinflammation; TRIMETHYLAMINE-N-OXIDE; ISCHEMIA/REPERFUSION INJURY; EXTRACELLULAR VESICLES; RISK-FACTORS; STROKE; MICROBIOTA; MICROGLIA; ACTIVATION; PROTECTS; PATHWAY;
D O I
10.3892/ijmm.2024.5354
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Stroke, a debilitating cerebrovascular ailment, poses significant threats to human life and health. The intricate interplay between the gut-brain-microbiota axis (GBMA) and cerebral ischemia-reperfusion has increasingly become a focal point of scientific exploration, emerging as a pivotal research avenue in stroke pathophysiology. In the present review, the authors delved into the nexus between the GBMA and neuroinflammation observed post-stroke. The analysis underscored the pivotal roles of histone deacetylase 3 and neutrophil extracellular traps subsequent to stroke incidents. The influence of gut microbial compositions and their metabolites, notably short-chain fatty acids and trimethylamine N-oxide, on neuroinflammatory processes, was further elucidated. The involvement of immune cells, especially regulatory T-cells, and the intricate signaling cascades including cyclic GMP-AMP synthase/stimulator of interferon genes/Toll-like receptor, further emphasized the complex regulatory mechanisms of GBMA in cerebral ischemia/reperfusion injury (CI/RI). Collectively, the present review offered a comprehensive perspective on the metabolic, immune and inflammatory modulations orchestrated by GBMA, augmenting the understanding of its role in neuroinflammation following CI/RI.
引用
收藏
页数:16
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