Klempt M, Klempt N D, Gluckman P D
Research Centre for Developmental Medicine and Biology, School of Medicine, University of Auckland, New Zealand.
Brain Res Mol Brain Res. 1993 Mar;17(3-4):347-50. doi: 10.1016/0169-328x(93)90021-g.
Brain halves were collected at various time points from 21-day-old Wistar rats exposed to either a short or prolonged period of inhalational hypoxia following unilateral carotid ligation post-insult. Neuronal loss was restricted to the side of the carotid ligation. Northern blot analysis was performed for IGFBP-2 mRNA. The prolonged hypoxia decreased the expression of IGFBP-2 five hours post insult, whereas the shorter insult level showed an (P < 0.05) increase above control. In both groups IGFBP-2 mRNA increased to peak 3-5 days post insult. After a decline at day 6, expression was again high 7-10 days after HI. In the short hypoxia group, where there was little neuronal loss, the expression of IGFBP-2 in both hemispheres followed the same pattern over time. However prolonged hypoxia induced higher IGFBP-2 expression in the ligated hemisphere where there was extensive neuronal loss. At day 5 post-insult 5/9 rats showed an additional, slightly smaller (1.4 kb vs 1.7 kb) second transcript. The different pattern of expression associated with different degrees of injury suggest that IGFBP-2 is involved in the post asphyxial response. Hypoxia itself leads to alterations in IGFBP-2 expression. Greater expression is associated with neuronal loss. These observations suggest that the IGF system contributes to neuronal rescue and/or brain repair processes.
在单侧颈动脉结扎损伤后，对暴露于短期或长期吸入性缺氧的21日龄Wistar大鼠在不同时间点采集脑半球。神经元损失局限于颈动脉结扎侧。对IGFBP-2 mRNA进行Northern印迹分析。长期缺氧在损伤后5小时降低了IGFBP-2的表达，而短期损伤组的表达水平比对照组增加（P<0.05）。两组中IGFBP-2 mRNA在损伤后3-5天均升高至峰值。在第6天下降后，HI后7-10天表达再次升高。在神经元损失很少的短期缺氧组中，两个半球中IGFBP-2的表达随时间遵循相同模式。然而，长期缺氧在有广泛神经元损失的结扎半球中诱导了更高的IGFBP-2表达。在损伤后第5天，5/9的大鼠显示出另外一个稍小（1.4 kb对1.7 kb）的第二条转录本。与不同程度损伤相关的不同表达模式表明IGFBP-2参与了窒息后反应。缺氧本身导致IGFBP-2表达改变。更高的表达与神经元损失相关。这些观察结果表明IGF系统有助于神经元拯救和/或脑修复过程。
