脑出血（ICH）发病率和死亡率居高不下，高压氧（HBO）广泛用于神经系统疾病的治疗，而对ICH患者是否具有益处仍有争议。我们前期研究发现HBO可加速清除ICH后血红蛋白（Hb）发挥抗炎保护效应，而IL-10缺失可使这些效应被部分阻断。结合近期文献，我们推测：HBO通过上调IL-10调控小胶质/巨噬细胞极化介导ICH后抗炎保护效应。本项目拟通过阐明下述问题以验证假说：①HBO是否通过Nrf2上调IL-10发挥抗炎保护效应；②IL-10/JAK1/STAT3途径诱导ICH后小胶质细胞M2型极化是否是HBO减轻炎症损伤发挥脑保护效应的关键机制；③ICH后外源性IL-10可否保护脑损伤；④上调CD163依赖的小胶质细胞吞噬效应是否是ICH后HBO加快Hb清除机制的关键效应环节。项目首次从调控小胶质细胞极化促进Hb清除为切入点探讨HBO的脑保护机制，有望为ICH损伤防治提供新思路。

The morbidity and mortality of intracerebral hemorrhage (ICH) remains high, and there is no effective means for prevention and treatment. HBO is widely used in the treatment of neurological diseases, but the benefits of ICH patients remain controversial. Our previous study found that HBO can suppress the neuro-inflammatory in acute phase after ICH and promote the hemoglobin(Hb) clearance, while the effects of HBO are reversed by IL-10 deficiency. In combination with recent literature, we speculated that HBO would increase IL-10 and further regulate the microglia/macrophage polarization, which mediated the neuroprotective effects. This project intends to clarify the following issues through the study in vivo and vitro in order to verify the hypothesis: ①whether HBO exert the neuroprotective effects by up-regulating expression of IL-10 through Nrf2. ②Whether HBO suppress neuroinflammation by promoting the M2-type microglial polarization after ICH through IL-10/JAK1/STAT3 pathway; ③Whether exogenous IL-10 can inhibit the excessive inflammatory response and protect the brain injury after ICH;④Whether the CD163-dependent microglial phagocytic function is the key mechanism of HBO in Hb removal after ICH. Together, the proposed studies will explore the underlying molecular mechanisms of enhanced Hb clearance and neuroprotection induced by HBO, and provide novel therapeutic strategies for ICH patients