Duanmu Wang-Sheng, Cao Liu, Chen Jing-Yu, Ge Hong-Fei, Hu Rong, Feng Hua
Department of Neurosurgery, General Hospital of Tibet Military Area Command, Lasa, China.
Department of Neurosurgery, Southwest Hospital of Third Military Medical University, Chongqing, China.
Neural Regen Res. 2016 Apr;11(4):641-5. doi: 10.4103/1673-5374.180751.
Ischemic postconditioning renders brain tissue tolerant to brain ischemia, thereby alleviating ischemic brain injury. However, the exact mechanism of action is still unclear. In this study, a rat model of global brain ischemia was subjected to ischemic postconditioning treatment using the vessel occlusion method. After 2 hours of ischemia, the bilateral common carotid arteries were blocked immediately for 10 seconds and then perfused for 10 seconds. This procedure was repeated six times. Ischemic postconditioning was found to mitigate hippocampal CA1 neuronal damage in rats with brain ischemia, and up-regulate acid-sensing ion channel 2a expression at the mRNA and protein level. These findings suggest that ischemic postconditioning up-regulates acid-sensing ion channel 2a expression in the rat hippocampus after global brain ischemia, which promotes neuronal tolerance to ischemic brain injury.
缺血后处理可使脑组织对脑缺血产生耐受，从而减轻缺血性脑损伤。然而，其确切作用机制仍不清楚。在本研究中，采用血管闭塞法对全脑缺血大鼠模型进行缺血后处理。缺血2小时后，立即阻断双侧颈总动脉10秒，然后再灌注10秒。此过程重复6次。结果发现，缺血后处理可减轻脑缺血大鼠海马CA1区神经元损伤，并在mRNA和蛋白水平上调酸敏感离子通道2a的表达。这些发现提示，全脑缺血后缺血后处理可上调大鼠海马中酸敏感离子通道2a的表达，从而促进神经元对缺血性脑损伤的耐受。
