Acidic preconditioning protects against ischemia-induced brain injury
Acidic preconditioning protects against ischemia-induced brain injury
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DOI：
10.1016/j.neulet.2012.05.015
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发表时间：
2012-08
影响因子：
2.5
通讯作者：
Chen-hui Zhang;Yan-Ying Fan;Xiao-fen Wang;J. Xiong;Ying Tang;Jieqiong Gao;Zhe Shen;Xiao-Hui Song;Jingying Zhang;Yao Shen;Qing Li;Xiangnan Zhang;Zhong Chen
中科院分区：
文献类型：
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作者：
Chen-hui Zhang;Yan-Ying Fan;Xiao-fen Wang;J. Xiong;Ying Tang;Jieqiong Gao;Zhe Shen;Xiao-Hui Song;Jingying Zhang;Yao Shen;Qing Li;Xiangnan Zhang;Zhong Chen
缺血预处理可预防脑缺血。最近的研究表明，酸性预处理（APC）对缺血诱导的心肌细胞损伤有保护作用。然而，APC是否对脑缺血具有保护作用尚不清楚。为了解决这个问题，我们将C57BL/6小鼠在含20%二氧化碳的常压环境中暴露3次，间隔10分钟，持续5分钟，然后进一步进行双侧颈总动脉闭塞。在被动回避实验中，APC改善了大鼠的表现，减少了海马CA1区的神经元损失，从而逆转了缺血引起的脑损伤。一致地，apc处理的脑切片和原代培养的神经元对氧葡萄糖剥夺（OGD）诱导的损伤的抵抗力更强，以pH和时间依赖的方式，正如逆转的细胞/组织活力所显示的那样。此外，APC处理可阻止ogd诱导的线粒体跨膜电位损失和凋亡，这一过程可被线粒体通透性转运开孔剂苍术苷抑制。综上所述，这些发现表明APC对缺血诱导的神经元损伤有保护作用。这种有益的效果可能至少部分归因于减少线粒体依赖性神经元凋亡。
Ischemic preconditioning protects against cerebral ischemia. Recent investigations indicated that acidic preconditioning (APC) protects against ischemia-induced cardiomyocytes injury. However, it is not clear whether APC can protect against cerebral ischemia. To address this issue, C57BL/6 mice were exposed 3 times at 10-min intervals to a normoxic atmosphere containing 20% CO2for 5min before being further subjected to bilateral common carotid artery occlusion. APC reversed the ischemia-induced brain injury as revealed by improved performance in passive avoidance experiments and decreased neuron loss in the hippocampal CA1 region. Consistently, both APC-treated brain slices and primary cultured neurons were more resistant to oxygen–glucose-deprivation (OGD)-induced injury, in a pH- and time-dependent manner, as revealed by reversed cell/tissue viability. In addition, the APC treatment prevented OGD-induced mitochondrial transmembrane potential loss and apoptosis, which was inhibited by the mitochondrial permeability transport pore opener atractyloside. Taken together, these findings indicated that APC protects against ischemia-induced neuronal injury. The beneficial effects may be attributed, at least in part, to decreased mitochondria-dependent neuronal apoptosis.