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.