一氧化碳中毒迟发性脑病（DEACMP）是急性一氧化碳中毒最严重的并发症，至今尚未发现有效的DEACMP的治疗方法。本课题组前期研究发现，辛伐他汀可抑制脑缺血再灌注损伤后自噬的过度激活，从而发挥神经保护作用。本课题拟在前期工作基础上，通过建立一氧化碳中毒细胞及动物模型，研究辛伐他汀干预一氧化碳中毒后，细胞自噬及BDNF/TrkB信号通路介导的脑组织细胞损伤变化情况，明确辛伐他汀干预自噬及BDNF/TrkB信号通路对一氧化碳中毒后脑组织损伤的保护作用及机制。本项目为一氧化碳中毒迟发性脑损伤的发病机制及制定相应诊疗方案提供理论依据。

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is the most severe complication of acute carbon monoxide (CO) poisoning. There is no cure for the disease, which worsens as it progresses, and eventually leads to death. Our preliminary study has found simvastatin can inhibit the over-activation of autophagy after cerebral ischemia-reperfusion injury, and thus play a role of neuroprotection. The study was designed to establish of CO poisoning cell and mice model, and determine the effect of simvastatin on CO poisoning induced autophagy and BDNF/TrkB signal pathway. We hope to find a new point of view to improve the brain function of patients after acute CO poisoning.