炎症反应在糖尿病缺血性脑卒中发病过程中发挥重要作用，而炎症相关干预靶点的缺乏导致新型抗炎症治疗方法研究进展缓慢。消退素D2（resolvin D2，RvD2）是新近发现的一类特化促消退介质，研究发现RvD2具有减轻炎症反应，促进血管再生等生物学功能。我们前期研究提示RvD2在糖尿病缺血性脑卒中患者外周血中显著降低，但其是否参与疾病的发生及其作用机制等至今未有报道。本项目在前期研究的基础上，利用临床患者样本及动物模型研究RvD2水平在糖尿病缺血性脑卒中发病中的变化，并在此基础上，通过升高RvD2水平及干扰RvD2作用通路探讨其对糖尿病缺血性脑卒中动物模型的神经存活的影响及其作用机制。研究结果不仅为糖尿病缺血性脑卒中的发病机制提供新的理论依据，更为深刻认识RvD2在其中作用的分子机制及研发靶向干预药物提供新的研究方向。

It is known that inflammation plays an important role in the pathogenesis of diabetic ischemic stroke. However, the lack of new intervention targets led to the slow progression in anti-inflammatory therapy in this disease. Resolvin D2 (RvD2) is a newly discovered of pro-resolving mediators, which has been reported to show the roles of anti-inflammation and regeneration of blood vessels. Although our previous study has found the significant decrease of RvD2 in the peripheral blood of diabetic ischemic stroke patients, little is known about the effects and mechanisms of reduced RvD2 in the progression of this disease. In this study, we will use patient sample and animal models to detect the alteration of RvD2 levels. Furthermore, by increasing the level of RvD2 or interfering with RvD2 related pathway, we investigated the effects of RvD2 on the neuron survival in the cell model or animal model of diabetic ischemic stroke. The results of our study will not only benefit for the understanding to the mechanisms of neuron damage in diabetic ischemic stroke but also improve the target therapy for this disease.