脑动静脉畸形是青少年颅内出血的重要病因，畸形团内微出血可诱导炎症反应，增加破裂出血风险。本课题旨在探讨脑动静脉畸形微出血向破裂出血转化过程中的炎症机制。研究假说提出：红细胞由脑动静脉畸形异常血管渗出，分解后铁沉积在影像学上表现为微出血灶，在铁沉积介导下，巨噬细胞MI/M2分化异常，破坏促炎/抗炎平衡，进一步损伤血管壁，导致畸形血管破裂出血。课题通过磁共振磁敏感序列检测微出血灶，对脑动静脉畸形进行分组，与组织学含铁血黄素沉着进行匹配；对畸形组织进行免疫荧光、流式细胞检测，分析巨噬细胞的表型和分泌炎症因子，并与血清炎症因子酶联免疫吸附测定结果及组织中炎症相关蛋白表达水平对比，探讨脑动静脉畸形微出血后，巨噬细胞失衡诱发的炎症反应与破裂出血的关系。

Brain arterivovenous malformaiton (BAVM) is an important risk factor of intracranial hemorrhage, especially in children and young adults. Microhemorrhages could induce inflammation and increased risk for rupture. This study aims to unravel inflammatory mechanism underling the course from microhemorrhage to symptomatic hemorrhage. A hypothesis is that erythrocyte extravasation secondary to the impaired vascular integrity of BAVM lead to iron deposition, which induce M1/M2 macrophage imbalance. The unrestrained proinflammatory phenotype will impair vessel wall which ultimately rupture. We detect microhemorrhage with susceptibility weighted image and match the results with histological findings. M1/M2 macrophage markers in tissue with or without silent/symptomatic hemorrhage are compared using immunofluorescence and flow cytometry. The results are further verified with the expression of inflammatory cytokines in serum and tissue using ELISA and protein chip. The identification of these molecular and cellular key players in BAVM hemorrhage may contribute to the development of novel therapies targeting this distinct macrophage population or iron deposition.