Gene and Protein Analysis on Ischemic Tolerance Caused by Focal Brain Lesioning

深部梨状皮质(DPC)是缺血性脑损伤的调节部位。我们研究了DPC破坏后脑内谷氨酸转运体(GLT-1、GLAST、EAAC-1)、钙离子非通透性谷氨酸受体亚单位(GluR2)和凋亡相关因子(bcl2、bax)基因和蛋白表达的机制。本研究的主要发现如下：(1)DPC损毁后，GLT-1、GluR2和BCL-2在海马区和皮质的基因和蛋白表达增加，而GLAST、EAAC-1和Bax的表达没有变化；(2)DPC损毁的脑缺血后，GLT-1、GluR2和bCL-2在海马区和皮质区的基因和蛋白表达增加；(3)DPC损毁后全脑缺血大鼠海马区存活细胞数增加，皮质梗塞体积扩大。因此，GLT-1、GluR2和bcl-2的上调分别导致谷氨酸摄取增加、低钙离子通透性增加和抗细胞凋亡，从而对脑缺血产生保护作用。

Deep prepiriform cortex (DPC) is the modulatory site for ischemic brain injury. We studied the mechanism on the gene and the protein expression about glutamate transporters (GLT-1, GLAST, EAAC-1), calcium ion non-permeable glutamate receptor subunit (GluR2) and apoptosis relating factors (bcl-2, bax) in the brain after DPC destruction. The major findings of this study are (1) Gene and protein expression in GLT-1, GluR2 and bcl-2 increased at the hippocampus and cortex after DPC destruction, however GLAST, EAAC-1 and bax were unchanged, (2) Gene and protein expression in GLT-1, GluR2 and bcl-2 increased at the hippocampus and cortex after ischemia in the DPC-destructed brain, and (3) The number of viable cell in the hippocampus increased in global ischemia and the volume of infarction in the cortex in focal ischemia in the DPC-destructed brain. Therefore up-regulation of GLT-1, GluR2 and bcl-2 each leads to increase of glutamate uptake, low calcium ion permeability and anti-apoptosis, then result in brain protection for ischemia.