The Interaction of Neutrophil Extracellular Traps and Complement in Intracerebral Hemorrhage

Intracerebral hemorrhage (ICH) is a prevalent cerebrovascular disease, which is an important cause of death and disability. Accumulating evidence indicates that the neutrophil extracellular traps (NETs) and complement cascade play an important role in the injury after ICH. Neutrophils, the first leukocyte subset recruited to the cerebral parenchyma following ICH, exacerbate cerebral tissue damage via the release of NETs. As a core component of the innate immune system, the complement system aggravates cerebral edema and pathological injury after ICH through a variety of complex pathological processes. Some complement molecules, such as C5a, C3a, and C1q, are associated with increased neutrophil recruitment and NETs release. Therefore, this review summarized the formation of NETs and activation of complement, the role of NETs and complement in ICH, the interaction between NETs and complement, and related treatment methods, providing new therapeutic strategies for clinical treatment.