With the advancement of endovascular therapy(EVT)techniques,the recanalization rate for patients with ischemic stroke(IS)has exceeded 80%.However,more than 50%of patients fail to achieve favorable neurological outcomes following recanalization,a phenomenon termed"futile recanalization"(FR).Neuroinflammation plays a pivotal role in the pathological progression of IS and is closely associated with the development of FR.This systematic review synthesizes the pivotal role of neuroinflammation in FR,encompassing three core pathological mechanisms:the no-reflow phenomenon,cerebral ischemia-reperfusion injury,and the gut-brain axis.The identification of various inflammation-related biomarkers shows promise for early detection of high-risk FR patients.Therapeutic agents including TLR4 antagonists(e.g.ApTOLL),neuroprotective compounds,and traditional Chinese medicine formulations demonstrate treatment potential through modulation of neuroinflammatory pathways.Targeted interventions against neuroinflammation may emerge as a strategic approach to improve clinical outcomes in IS patients.

With the advancement of endovascular therapy(EVT)techniques,the recanalization rate for patients with ischemic stroke(IS)has exceeded 80%.However,more than 50%of patients fail to achieve favorable neurological outcomes following recanalization,a phenomenon termed"futile recanalization"(FR).Neuroinflammation plays a pivotal role in the pathological progression of IS and is closely associated with the development of FR.This systematic review synthesizes the pivotal role of neuroinflammation in FR,encompassing three core pathological mechanisms:the no-reflow phenomenon,cerebral ischemia-reperfusion injury,and the gut-brain axis.The identification of various inflammation-related biomarkers shows promise for early detection of high-risk FR patients.Therapeutic agents including TLR4 antagonists(e.g.ApTOLL),neuroprotective compounds,and traditional Chinese medicine formulations demonstrate treatment potential through modulation of neuroinflammatory pathways.Targeted interventions against neuroinflammation may emerge as a strategic approach to improve clinical outcomes in IS patients.

Objective To investigate the gut microbial characteristics in patients with acute ischemic stroke and resilience of the gut microbiota after a stroke. Methods Ninety-five fecal samples from 28 ischemic stroke patients and 28 fecal samples from 28 healthy volunteers were collected.DNA was extracted from these samples and the bacterial 16S rRNA were amplified through real-time quantitative polymerase chain reaction (qPCR). All PCR products were mixed together and then sequenced using the Illumina Hiseq 2500 platform. Microbiome analysis was implemented in QIIME. Results Patients with acute ischemic stroke showed significantly higher diversity than controls (phylogenetic diversity, P=0.002). The overall composition of the gut microbial communities also differed significantly between acute ischemic stroke patients and healthy controls as indicated by the clear separation in principle coordinate analysis (Adonis test on Bray-Curtis, P<0.001). Stroke patients' intestines had more opportunistic pathogens, such as Enterobacteriaceae, Veillonellaceae and Streptococcaceae, fewer commensal or beneficial genera including Bacteroides and Prevotella. Four weeks after onset, the gut microbiota in stroke patients began to restore, but the alpha diversity declined (P<0.05). Conclusion The present study has revealed the characteristic of gut microbial dysbiosis and recovery in acute ischemic stroke patients.However,the significance of the dynamic gut microbiota in stroke patients needs further study.