Alteration of insulin-like growth factor-1 expression after middle cerebral artery occlusion in monkeys and rats: complementary DNA microarray, immunohistochemistry, and in situ hybridization studies.
Alteration of insulin-like growth factor-1 expression after middle cerebral artery occlusion in monkeys and rats: complementary DNA microarray, immunohistochemistry, and in situ hybridization studies.
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DOI：
10.1016/j.jstrokecerebrovasdis.2006.05.011
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发表时间：
2006-07-01
期刊：
影响因子：
--
通讯作者：
Wang, Chao
中科院分区：
文献类型：
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作者：
Gao, Huanmin;Liu, Yaoquan;Wang, Chao
胰岛素样生长因子（IGF）-1在大鼠和绵羊脑缺血模型中具有明显的神经保护作用。为探讨IGF-1对脑缺血损伤是否具有神经保护作用，本研究作为亚人灵长类动物脑缺血系列研究的一部分，观察了猴和大鼠大脑中动脉闭塞后IGF-1 mRNA和蛋白的表达。共使用12，800点互补DNA微阵列、原位杂交和免疫组织化学。互补DNA微阵列显示，在近8000个基因中，约8%的基因在缺血/再灌注损伤后受到影响，特别是在缺血区域的生长因子家族，包括IGF-1。缺血24 h后，岛纹状体IGF-1 mRNA和蛋白表达降低，海马IGF-1 mRNA表达增加，蛋白表达无变化。结果提示，IGF-1可能以不同于大鼠的方式参与神经保护通路，对猴局灶性脑缺血后缺血损伤的神经细胞具有保护作用。
It is well established that insulin-like growth factor (IGF)-1 has potent neuroprotective effects on cerebral ischemia in the rat and sheep model. In order to investigate whether it has neuroprotective effects on brain insult in human stroke, as one part of serial subhuman primate stroke research, the present study was designed to observe whether IGF-1 messenger RNA (mRNA) and protein is expressed in middle cerebral artery occlusion in monkeys and rats. A total of 12,800 dots complementary DNA microarray, in situ hybridization, and immunohistochemistry were used. Complementary DNA microarray showed that among the nearly 8000 genes, approximately 8% of the total number of genes examined was affected after ischemia/reperfusion injury especially in the growth factor family including IGF-1 in the ischemic region. The decreased IGF-1 mRNA and protein expression was found in the insular striatum, but there was an increased mRNA expression and unchanged protein expression in the hippocampus 24 hours after ischemia. The results suggested that IGF-1 might contribute to the neuroprotective pathway in a pattern different from that of rats, and it might play a role in protection of ischemic injured neuronal cells after monkey focal cerebral ischemia.