Research Equipment Center, Hamamatsu University School of Medicine, 1-20-1Handayama, Higashiku, Hamamatsu, 431-3192, Japan.
J Mol Neurosci. 2013 Feb;49(2):320-7. doi: 10.1007/s12031-012-9830-5. Epub 2012 Jun 15.
Neonatal hypoxic-ischemic (HI) encephalopathy can lead to severe brain damage and is a common cause of neurological handicaps in adulthood. To elucidate the molecular events occurring in cerebral cortices of mature rats (8 weeks old) after neonatal HI brain insult, we performed comprehensive gene expression and gene network analyses using a DNA microarray system (Agilent 4x44K). A rat model of neonatal HI encephalopathy (Rice model) was obtained by unilateral ligation of the common carotid artery of 7-day-old rats with hypoxia (exposure to 8 % oxygen). Due to the HI insult-related breakdown of the ipsilateral hemisphere in the brain, RNAs were prepared from the contralateral cerebral cortices of 8-week-old rats and analyzed by DNA microarray. Biofunctional analysis of differentially regulated genes revealed that many upregulated genes were related to cell death signaling, such as the arachidonic acid cascade. In contrast, many downregulated genes were related to gene expression, reflecting progressive damage by the HI insult, even within the contralateral cerebral hemisphere.
新生儿缺氧缺血性（HI）脑病可导致严重的脑损伤，是成年期神经功能障碍的常见原因。为了阐明新生 HI 脑损伤后成熟大鼠（8 周龄）大脑皮质中发生的分子事件，我们使用 DNA 微阵列系统（Agilent 4x44K）进行了全面的基因表达和基因网络分析。通过对 7 天大的大鼠单侧结扎颈总动脉并缺氧（暴露于 8%氧气）获得新生儿 HI 脑病大鼠模型（Rice 模型）。由于 HI 损伤导致大脑同侧半球破裂，我们从 8 周龄大鼠的对侧大脑皮质中提取 RNA，并通过 DNA 微阵列进行分析。差异调控基因的生物功能分析表明，许多上调的基因与细胞死亡信号有关，如花生四烯酸级联。相比之下，许多下调的基因与基因表达有关，反映了 HI 损伤的进行性损伤，即使在对侧大脑半球也是如此。
