脑室出血后继发交通性脑积水较为常见，且与患者神经功能预后不良显著相关。研究发现红细胞降解产物与脑室出血后继发交通性脑积水关系密切，抑制/清除红细胞降解产物有助于减缓出血后交通性脑积水的发生发展。但红细胞降解产物成分复杂，其中主要致病物质及致伤机制尚缺乏全面深入研究。.前期工作发现：红细胞中含量丰富的Peroxiredoxin2（Prx2）蛋白在脑室穿刺注射后可加剧继发交通性脑积水并诱发脑室相关组织的炎性反应。据此，本项目拟利用大鼠脑室穿刺注射模型，通过注射冻融红细胞及自体血模拟脑室出血病程，验证Prx2蛋白在脑室出血后继发交通性脑积水中的作用并阐明其具体效应途径，从而完善脑室出血后继发交通性脑积水的发病机制并寻找潜在治疗靶点。

Communicating hydrocephalus following intraventricular hemorrhage (IVH) is quite common and shows significant correlation with unfavorable prognosis. Researches have found intimate connections between secondary communicating hydrocephalus following IVH and red blood cell （RBC）lysis, while suppression/elimination of RBC lysis could attenuate such a pathological process. However, due to the complexity of RBC lysis, the major pathogenic compositions it contains and their acting mechanisms still need further study..Peroxiredoxin 2 (Prx2) protein, which is rich in the cytoplasm of RBC, has been proved influential in the development of communicating hydrocephalus after intraventricular injection. Evidence also indicates significant inflammatory response of the ventricular tissue after Prx2 protein injection. Hereby, this research was designed to verify the specific role of Prx2 protein in the development of secondary communicating hydrocephalus following IVH and its pathologic mechanism. A rat Lysed-RBC/Autologous blood intraventricular injection model will be employed in this research to better simulate the clinical course of IVH. Achievements of this research could help to replenish the pathogenesis of secondary communicating hydrocephalus following IVH and indicate potential therapeutic targets.