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Acidic preconditioning protects against ischemia-induced brain injury

机译:酸性预处理可预防缺血性脑损伤

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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% CO 2 for 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.
机译:缺血预处理可预防脑缺血。最近的研究表明,酸性预处理(APC)可防止缺血引起的心肌细胞损伤。但是,尚不清楚APC是否可以预防脑缺血。为了解决这个问题,在进一步使双侧颈总动脉闭塞之前,将C57BL / 6小鼠以10分钟的间隔暴露于含20%CO 2的常氧环境中3次,持续5分钟。 APC通过改善被动回避实验的性能和减少海马CA1区神经元的丢失来逆转缺血性脑损伤。一致地,APC处理过的脑切片和原代培养的神经元都对pH值和时间依赖性的氧葡萄糖剥夺(OGD)诱导的损伤具有更强的抵抗力,如逆转的细胞/组织活力所揭示。此外,APC处理可防止OGD诱导的线粒体跨膜电位损失和凋亡,这被线粒体通透性转运开孔剂白术苷抑制。综上,这些发现表明APC可以防止缺血引起的神经元损伤。有益作用可以至少部分归因于线粒体依赖性神经元凋亡的减少。

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