一氧化碳中毒是我国发病和死亡人数最多的急性职业中毒，一氧化碳中毒迟发性脑病（DEACMP）是其最严重的并发症。本项目组前期研究发现GRb1可抵抗由CO中毒引起的神经元死亡与抑制过度自噬相关，从而发挥脑保护的作用。我们拟通过一氧化碳中毒模型的建立，探索了自噬对神经元损伤的影响和GEF-H1通路对一氧化碳中毒后神经元可塑性功能恢复的影响，人参皂甙Rb1的干预作用和机制研究；本课题将为一氧化碳中毒的分子生物学机制提供新的理论依据，有望为一氧化碳中毒提供新的治疗靶点。

Carbon monoxide (CO) poisoning is an acute occupational poisoning of the highest morbidity and mortality in China, the incidence of its most serious complication which named delayed encephalopathy after acute carbon monoxide poisoning (DEACMP).Our preliminary study has found that, GRb1 resistance to CO poisoning caused by neuronal death, and curb excessive autophagy-related，and thus play a role of neuroprotectionThrough the establishment of carbon monoxide poisoning model to explore the effects of Synaptic plasticity after DEACMP functional recovery of the intervention of GRb1 and mechanisms of autophagy research on neuronal injury and GEF-H1 pathway; Thisproject will provide a new theoretical molecular mechanism of DEACMP, andpotentially lead to a therapeutic breakthrough.