缺血后适应可减轻脑缺血再灌注损伤，且在再灌注开始后干预，比缺血预适应更符合治疗特点。但缺血后适应对脑缺血的保护机制不清,我们前期研究发现：脑缺血后适应可明显减轻脑缺血再灌注损伤，改善神经功能缺失；芯片筛查结果发现脑缺血后适应可显著降低脑缺血再灌注后细胞周期蛋白mRNA表达的增加；且对蛋白激酶、转录因子等有较大影响,并且我们进一步验证了细胞周期蛋白的表达。针对脑缺血后适应对脑缺血再灌注保护机制不清，以及我们前期发现，提出假设：脑缺血后适应对脑缺血的保护作用从影响蛋白激酶的活性开始，通过调控转录因子的表达和活性来调控多种神经细胞的细胞周期蛋白的表达。我们将应用大鼠和非人灵长类动物为模型，应用免疫共沉淀、基因转染技术、流式细胞检测技术等探索脑缺血后适应的保护及其分子机制问题，对阐明缺血再灌注后多种神经细胞的增殖规律以及缺血后适应对其影响的规律有重要意义，为缺血性脑血管病神经保护治疗策略提供思路。

Ischemic postconditioning could alleviate the ischemia and reperfusion injury, which was performed after ischemia and reperfusion, then was more applicable to clinical practice than ischemic preconditioning. However,the machanism is unclear. Our previous study showed that cerebral ischemic postconditioning decreased the ischemia and reperfusion injuries. Our Affymetrix gene-chip data and further confirmation study showed that ischemic postconditioning significantly reduced the expression of cell cycle proteins, and also have great influence on protein kinases and transcriptor factors. Based on our primilitary foundation and the unclear underlying mechanism of neuroprotective effect of cerebral ischemic postconditioning, we hypothesesed that the neuroprotection of ischemic postconditioning is initiated by affecting the activity of some protein kinases, and probably via the expression of transcription factors to regulate the expression of cell cycle proteins.We are going to carry out research by using the rat and monkey animal model, lentivirus infection, RNA interference, to demonstrate the time-dependent proliferation of different kinds of neural cells after ischemia/reperfusion and the underlying mechanisms, providing the basic researches for the clinical transformation of ischemic preconditioning, and explored the new therapeutic strategy for cerebral ischemia and reperfusion.