脑缺血/低氧预适应(I/HPC)是缺血/低氧预刺激诱发的一种内源性神经保护现象。这一现象的发现为临床缺血性脑疾病的防治提供了新思路，但其发生发展的确切细胞信号转导机制尚不清楚。我们前期工作发现，经典蛋白激酶C(cPKC)betaII、gamma 及新奇型PKC (nPKC)epsilon三亚型的118个相互作用蛋白，以及19个差异表达miRNAs参与了脑I/HPC 的形成，初步预测了差异表达miRNAs-PKC亚型特异性信号蛋白网络。本课题拟利用小鼠整体I/HPC和脑中动脉阻塞致局部缺血性卒中模型，进一步验证PKC 亚型特异性相互作用蛋白与脑损伤程度的关系，阐明特定miRNA-PKC亚型特异性相互作用蛋白信号网络在脑缺血/低氧性损伤和保护中作用。所获成果将进一步丰富人们对脑I/HPC形成机制的认识并指导临床。

Ischemic/hypoxic preconditioning (I/HPC) is a phenomenon of ischemia/hypoxia pretreatment-evoked endogenous neuroprotection, which may provide new idea for the prevention and treatment of ischemic/hypoxic injuries-related brain disease. Unfortunately the accurate signal transduction mechanism of I/HPC is not clear. Our previous reports have confirmed that the classical protein kinase C (cPKC) betaII, gamma and novel PKC (nPKC) epsilon-interacting proteins, and 19 differentially expressed miRNAs were involved in the cerebral I/HPC development. Based on the network prediction of specified miRNAs-PKC isoform-specific signaling pathways, we will further explore the formation of cPKC interacting protein involved in the HPC，the correlation of PKC isoform-specific interacting proteins with the degree of cerebral injuries, and the role of miRNAs-PKC isoform-specific signaling pathways in brain ischemic/hypoxic injuries and neuroprotection by using I/HPC and middle cerebral artery occlusion (MCAO)-induced ischemic stroke mouse models.