Mechanisms in Adaptation to Brain Ischemia by Ischemic Preconditioning

Abstract

During the last few years, the mechanisms of adaptation to brain ischemic preconditioning (IPC) of cerebral ischemia/reperfusion have been studied and various molecules and a number of molecular regulation pathways were proposed to participate in IPC. Better understanding of mechanisms in IPC may provide novel therapeutic interventions for preventive treatment of cerebral ischemia. Since mitochondria are the most important intracellular energy source and are crucial for the cells' survival in the occurrence of ischemia, so more attention should be paid to the investigation of mitochondria related mechanisms of IPC. In this review, we will first survey the mitochondria related mechanisms including mitochondrial apoptotic pathway, uncoupling protein 2 (UCP2), mitochondria deprived reactive oxygen species (ROS), and mitochondrial ATPsensitive K(superscript +) channels (MitoKATP) in postischemic neuroprotection in brain. Then, to be more comprehensive, the mitochondria non-related mechanisms such as N-methyl-D-aspartate (NMDA) and Gamma-aminobutyric acid (GABA) receptors, adenosine, adenosine A1 receptor and K(superscript +) channels as well as nitric oxide will also be reviewed.