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新生大鼠脑缺氧缺血后c-fos信使核糖核酸的变化

Changes in c-fos mRNA in the neonatal rat brain following hypoxic ischemia.

作者信息

Adén U, Bona E, Hagberg H, Fredholm B B

机构信息

Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.

出版信息

Neurosci Lett. 1994 Oct 24;180(2):91-5. doi: 10.1016/0304-3940(94)90495-2.

DOI:10.1016/0304-3940(94)90495-2
PMID:7700600
Abstract

We used quantitative in situ hybridization to study changes in the expression of c-fos following hypoxic-ischemia (H-I) in the neonatal rat brain. 7-day-old rat pups were subjected to a unilateral ligation of the common carotid artery followed by a 2 h 15 min hypoxic period (7.7% O2 in N2). This resulted in the expected ipsilateral infarction of cortex, lateral hippocampus, lateral-superior aspects of the striatum and the white matter of the corpus callosum. Brain damage was not seen in the contralateral hemisphere subjected only to hypoxia. c-fos mRNA levels increased in the contralateral hemisphere immediately after the hypoxia and had returned towards normal levels 2 h thereafter. In the ipsilateral hemisphere, the expression of c-fos was delayed but very marked at 2 h. Animals subjected only to hypoxia showed little or no increase in c-fos mRNA. Thus the earliest recorded increase in c-fos after hypoxic ischemia, which occurred on the non-ischemic, contralateral side, may represent a generalized response to a more localized insult.

摘要

我们采用定量原位杂交技术,研究新生大鼠脑缺氧缺血(H-I)后c-fos表达的变化。对7日龄的幼鼠进行单侧颈总动脉结扎,随后进行2小时15分钟的缺氧处理(氮气中含7.7%氧气)。这导致了预期的同侧皮质、外侧海马、纹状体外侧上部以及胼胝体白质梗死。仅经历缺氧的对侧半球未见脑损伤。缺氧后立即,对侧半球的c-fos mRNA水平升高,并在2小时后恢复至正常水平。在同侧半球,c-fos的表达延迟,但在2小时时非常明显。仅经历缺氧的动物c-fos mRNA几乎没有增加或没有增加。因此,缺氧缺血后最早记录到的c-fos增加发生在非缺血的对侧,这可能代表了对更局部损伤的全身性反应。

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Changes in c-fos mRNA in the neonatal rat brain following hypoxic ischemia.新生大鼠脑缺氧缺血后c-fos信使核糖核酸的变化
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[Time-course of mu-calpain activation, c-Fos, c-Jun, HSP70 and HSP27 expression in hypoxic-ischemic neonatal rat brain].[新生大鼠缺氧缺血性脑损伤中μ-钙蛋白酶激活、c-Fos、c-Jun、热休克蛋白70和热休克蛋白27表达的时间进程]
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Is Fos protein expressed by dying striatal neurons after immature hypoxic-ischemic brain injury?未成熟脑缺氧缺血性损伤后,死亡的纹状体神经元是否表达Fos蛋白?
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Differential activation of c-fos and caspase-3 in hippocampal neuron subpopulations following neonatal hypoxia-ischemia.新生期缺氧缺血后海马神经元亚群中c-fos和caspase-3的差异激活
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Neuroprotective action of cycloheximide involves induction of bcl-2 and antioxidant pathways.
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