免疫炎症反应参与了急性一氧化碳中毒迟发性脑病（DEACMP）的发病过程，HMGB1/TLR4/NF-κB通路在机体免疫炎症反应过程中起着至关重要的作用，通路上的关键信号分子均能直接或间接激发炎症反应的发生与发展。本课题组前期研究表明：（1）促红细胞生成素可降低大鼠脑缺血再灌注损伤后NF-κB、TNF-α的表达，从而发挥神经保护作用；（2）早期应用促红细胞生成素有助于急性一氧化碳中毒患者的神经功能恢复，并能降低DEACMP的发生率。本课题拟在前期工作基础上，采用大鼠DEACMP模型首次研究DEACMP大鼠脑内HMGB1的动态变化及对下游TLR4/NF-κB的影响；观察不同剂量促红细胞生成素对DEACMP大鼠脑内HMGB1/TLR4/NF-κB通路及相关免疫炎症因子的抑制作用，解析促红细胞生成素对DEACMP神经保护的分子机制及作用靶点，为DEACMP患者的救治开辟新的理论基础及治疗方法。

Immune inflammatory reaction involved in the pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), HMGB1/TLR4/NF-κB pathway plays a crucial role in the course of immune and inflammation, the key signaling molecules on the pathways can directly or indirectly stimulate the development of inflammatory response. Our preliminary study has found：(1) Erythropoietin can reduce the expression of NF-κB and TNF-α in rats of cerebral ischemia-reperfusion injury, and thus play a role of neuroprotection. (2) Early administration of erythropoietin to patients with CO poisoning improved neurological outcomes and reduced the incidence of DEACMP. The project intends to investigate the dynamic changes of HMGB1 in DEACMP rat brain and the impact on downstream TLR4/NF-κB pathway. By observing different doses of erythropoietin inhibit HMGB1/TLR4/NF-κB pathway and immune inflammatory factors in DEACMP rat brain, we would analyze neuroprotection molecular mechanisms and protect targets of erythropoietin, opening up new theoretical foundation and treatment method for DEACMP patients.