脑出血作为脑卒中一种严重的疾病类型，具有极高的致残率和死亡率，然而目前尚无有效的药物治疗。我们的前期研究及以往研究显示清道夫分子CD163在脑出血模型中特异性表达上调，与预后相关，且表达于中枢小胶质细胞、星形胶质细胞、神经元等细胞的表面，其表达趋势与脑损伤趋势一致。本课题拟借助野生小鼠和基因敲除、过表达小鼠脑出血模型并结合在体、离体实验对脑出血后CD163作用机制进行探索。我们假设脑出血后，CD163通过介导红细胞裂解产物清除并发挥免疫调节功能减轻脑水肿进展，从而减轻神经功能损伤。因此，本项目拟研究：1）CD163对脑出血后血肿及血肿周围水肿进展的影响2）CD163对脑出血后红细胞裂解产物的影响3）CD163对脑出血后免疫反应的影响4）针对CD163的干预探索。本项目旨在探索CD163对出血性脑卒中的作用机制，为脑出血防治提供新靶点。

Intracerebral hemorrhage as a severe subtype of stroke, always has high morbidity and mortality, while effective therapies are still in great need. Our and other previous studies have shown that scavenger receptor CD163 was up-regulated after animal model of intracerebral hemorrhage and correlated with prognosis, which also expressed in central microglia，astrocytes and neurons, and its expression trend was consistent with that of brain injury. This project aims to investigate the functioning mechanism of CD163 after intracerebral hemorrhage by using wild-type and gene knockout and overexpression mouse model of intracerebral hemorrhage both in vivo & in vitro. We hypothesized that after intracerebral hemorrhage, CD163 can mediate the phagocytosis of red blood cell lysis components and modulate immune response after ICH, thus relief brain edema and neurological deficits. Therefore, this project intends to study: (1) Function of CD163 on hematoma clearance and peri-hematoma edema progression after intracerebral hemorrhage (2) Influence of CD163 on red blood cells lysis product (3) The effect of CD163 on the immune response after intracerebral hemorrhage (4) Possible intervention focus on CD163. The purpose of this project is to explore the functioning mechanism of CD163 in intracerebral hemorrhage, thus provide novel target for treatment of intracerebral hemorrhage.