Ding Zhe-Min, Wu Bing, Zhang Wei-Qiao, Lu Xiao-Jie, Lin Yu-Chang, Geng Yong-Jian, Miao Yi-Feng
Neuroscience Center, Wuxi No. 2 Hospital, Nanjing Medical University, Wuxi 214002, China.
Department of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Int J Mol Sci. 2012;13(5):6089-6101. doi: 10.3390/ijms13056089. Epub 2012 May 18.
Transient forebrain or global ischemia induces neuronal death in vulnerable CA1 pyramidal cells with many features. A brief period of ischemia, i.e., ischemic preconditioning, or a modified reperfusion such as ischemic postconditioning, can afford robust protection of CA1 neurons against ischemic challenge. Therefore, we investigated the effect of ischemic preconditioning and postconditioning on neural cell apoptosis in rats. The result showed that both ischemic preconditioning and postconditioning may attenuate the neural cell death and DNA fragment in the hippocampal CA1 region. Further western blot study suggested that ischemic preconditioning and postconditioning down-regulates the protein of cleaved caspase-3, caspase-6, caspase-9 and Bax, but up-regulates the protein Bcl-2. These findings suggest that ischemic preconditioning and postconditioning have a neuroprotective role on global brain ischemia in rats through the same effect on inhibition of apoptosis.
短暂性前脑或全脑缺血会导致易损的CA1锥体细胞出现多种特征的神经元死亡。短暂的缺血期,即缺血预处理,或如缺血后处理等改良的再灌注,能够为CA1神经元提供强大的保护,使其免受缺血挑战。因此,我们研究了缺血预处理和后处理对大鼠神经细胞凋亡的影响。结果显示,缺血预处理和后处理均可减轻海马CA1区的神经细胞死亡和DNA片段化。进一步的蛋白质印迹研究表明,缺血预处理和后处理下调了裂解的半胱天冬酶-3、半胱天冬酶-6、半胱天冬酶-9和Bax的蛋白表达,但上调了Bcl-2蛋白。这些发现表明,缺血预处理和后处理通过对细胞凋亡抑制的相同作用,对大鼠全脑缺血具有神经保护作用。