Ischemic preconditioning with non‐lethal ischemia can be protective against lethal forebrain ischemia. We hypothesized that aging may aggravate ischemic susceptibility and reduce brain plasticity against preconditioning. Magnetic resonance diffusion tensor imaging (DTI) is a sensitive tool to detect brain integrity and white matter architecture. This study used DTI and histopathology to investigate the effect of aging on ischemic preconditioning. In this study, adult and middle‐aged male Mongolian gerbils were subjected to non‐lethal 5‐min forebrain ischemia (ischemic preconditioning) or sham‐operation, followed by 3 days of reperfusion, and then lethal 15‐min forebrain ischemia. A 9.4‐Tesla MR imaging system was used to study DTI indices, namely fractional anisotropy (FA), mean diffusivity (MD), and intervoxel coherence (IC) in the hippocampal CA1 and dentate gyrus (DG) areas. In situ expressions of microtubule‐associated protein 2 (MAP2, dendritic marker protein) and apoptosis were also examined. The 5‐min ischemia did not cause dendritic and neuronal injury and any significant change in DTI indices and MAP2 in adult and middle‐aged gerbils. The 15‐min ischemia‐induced significant delayed neuronal apoptosis and early dendritic injury evidenced by DTI and MAP2 studies in both CA1 and DG areas with more severe injury in middle‐aged gerbils than adult gerbils. Ischemic preconditioning could improve neuronal apoptosis in CA1 area and dendritic integrity in both CA1 and DG areas with better improvement in adult gerbils than middle‐aged gerbils. This study thus suggests an age‐dependent protective effect of ischemic preconditioning against both neuronal apoptosis and dendritic injury in hippocampus after forebrain ischemia.

中文翻译：

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缺血预处理对海马神经元凋亡和树突状损伤的保护作用是年龄依赖性的。

非致命性缺血的缺血预处理可以预防致命的前脑缺血。我们假设衰老可能会加重缺血敏感性，并降低大脑对可适应性的可塑性。磁共振扩散张量成像（DTI）是检测大脑完整性和白质结构的灵敏工具。这项研究使用DTI和组织病理学来研究衰老对缺血预处理的影响。在这项研究中，成年和中年男性蒙古沙鼠经历了非致命的5分钟前脑缺血（缺血预处理）或假手术，然后再灌注3天，然后致命的15分钟前脑缺血。使用9.4-Tesla MR成像系统研究DTI指标，即分数各向异性（FA），平均扩散率（MD），和海马CA1区和齿状回（DG）区的体素间连贯性（IC）。还检查了微管相关蛋白2（MAP2，树突标记蛋白）的原位表达和细胞凋亡。5分钟局部缺血不会引起树突状和神经元损伤，并且在成年和中年沙鼠中DTI指数和MAP2均无任何显着变化。DTI和MAP2研究在CA1和DG地区进行的15分钟局部缺血诱导的明显神经元凋亡和早期树突状损伤证明，中年沙鼠的伤害比成年沙鼠更严重。缺血预处理可以改善CA1区的神经元凋亡和CA1区和DG区的树突完整性，其中成年沙鼠比中年沙鼠更好。