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首页> 外文期刊>Brain research >The temporal profile of genomic responses and protein synthesis in ischemic tolerance of the rat brain induced by repeated hyperbaric oxygen.
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The temporal profile of genomic responses and protein synthesis in ischemic tolerance of the rat brain induced by repeated hyperbaric oxygen.

机译：反复高压氧诱导大鼠脑缺血耐受中基因组反应和蛋白质合成的时间变化

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摘要

Repeated hyperbaric oxygen (HBO) exposure prior to ischemia has been reported to provide neuroprotection against ischemic brain injury. The present study examined the time course of neuroprotection of HBO (3.5 atmosphere absolute, 100% oxygen, 1 h for 5 consecutive days) and the changes of gene/protein expression in rats. First, at 6 h, 12 h, 24 h, and 72 h after HBO sessions, rats were subjected to forebrain ischemia (8 min). Histopathological examination of hippocampal CA1 neurons was done 7 days after ischemia. Second, temporal genomic responses and protein expression were examined at the same time points after HBO sessions without subjecting animals to ischemia. HBO significantly reduced loss of hippocampal CA1 neurons that normally follows transient forebrain ischemia when the last HBO session was 6 h, 12 h, or 24 h before ischemia (survived neurons 55%, 75%, and 53%, respectively), whereas if there was a 72-h delay before the ischemic insult, HBO was not protective (survived neurons only 6%). Statistical analysis on microarray data showed significant upregulation in 60 probe sets including 7 annotated genes (p75NTR, C/EBPdelta, CD74, Edg2, Trip10, Nrp1, and Igf2), whose time course expressions corresponded to HBO-induced neuroprotection. The protein levels of p75NTR, C/EBPdelta, and CD74 were significantly increased (maximum fold changes 2.9, 2.0, and 7.9, respectively). The results suggest that HBO-induced neuroprotection against ischemic injury has time window, protective at 6 h, 12 h and 24 h but not protective at 72 h. Although the precise interaction is to be determined, the genes/proteins relevant to neurotrophin and inflammatory-immune system may be involved in HBO-induced neuroprotection.
机译：据报道，在缺血之前反复暴露高压氧（HBO）可提供针对缺血性脑损伤的神经保护作用。本研究检查了HBO的神经保护作用的时间过程（3.5个大气压绝对压力，100％氧气，连续5天为1小时）以及大鼠中基因/蛋白质表达的变化。首先，在HBO治疗后6小时，12小时，24小时和72小时，对大鼠进行前脑缺血（8分钟）。缺血7天后进行海马CA1神经元的组织病理学检查。其次，在HBO治疗后的同一时间点检查时间基因组反应和蛋白质表达，而不使动物遭受局部缺血。当最后一次HBO疗程为缺血前6 h，12 h或24 h时，HBO可以显着减少通常在短暂性前脑缺血后海马CA1神经元的丢失（存活的神经元分别为55％，75％和53％），而如果存在在缺血性损伤之前延迟了72小时，HBO没有保护作用（存活的神经元只有6％）。对微阵列数据的统计分析显示，在60个探针组中有显着上调，包括7个带注释的基因（p75NTR，C / EBPdelta，CD74，Edg2，Trip10，Nrp1和Igf2），其时程表达与HBO诱导的神经保护相对应。 p75NTR，C / EBPdelta和CD74的蛋白质水平显着增加（最大倍数变化分别为2.9、2.0和7.9）。结果表明，HBO诱导的针对缺血性损伤的神经保护具有时间窗，在6 h，12 h和24 h有保护作用，但在72 h没有保护作用。尽管确定精确的相互作用，但是与神经营养蛋白和炎性免疫系统有关的基因/蛋白可能参与HBO诱导的神经保护。

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