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慢性产前缺氧后的皮质神经元丢失:一项对比性实验室研究。

Cortical neuronal loss after chronic prenatal hypoxia: a comparative laboratory study.

作者信息

Chung Yoon Young, Jeon Yong Hyun, Kim Seok Won

机构信息

Department of Anatomy, School of Medicine, Chosun University, Gwangju, Korea.

Department of Neurosurgery, School of Medicine, Chosun University, Gwangju, Korea.

出版信息

J Korean Neurosurg Soc. 2014 Dec;56(6):488-91. doi: 10.3340/jkns.2014.56.6.488. Epub 2014 Dec 31.

DOI:10.3340/jkns.2014.56.6.488
PMID:25628808
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4303724/
Abstract

OBJECTIVE

The purpose of this study was to investigate the prenatal hypoxic effect on the fetal brain development.

METHODS

We used the guinea pig chronic placental insufficiency model to investigate the effect of hypoxia on fetal brain development. We ligated unilateral uterine artery at 30-32 days of gestation (dg : with term defined as -67 dg). At 50 dg, 60 dg, fetuses were sacrificed and assigned to either the growth-restricted (GR) or control (no ligation) group. After fixation, dissection, and sectioning of cerebral tissue from these animals, immunohistochemistry was performed with NeuN antibody, which is a mature neuronal marker in the cerebral cortex.

RESULTS

The number of NeuN-immunoreactive (IR) cells in the cerebral cortex did not differ between the GR and control groups at 50 dg. However, the number of NeuN-IR cells was lesser in GR fetuses than in controls at 60 dg (p<0.05).

CONCLUSION

These findings show that chronic prenatal hypoxia affect the number of neuron in the cerebral cortex of guinea pig fetus at 60 dg. The approach used in this study is helpful for extending our understanding of neurogenesis in the cerebral cortex, and the findings may be useful for elucidating the brain injury caused by prenatal hypoxia.

摘要

目的

本研究旨在探讨产前缺氧对胎儿脑发育的影响。

方法

我们使用豚鼠慢性胎盘功能不全模型来研究缺氧对胎儿脑发育的影响。在妊娠30 - 32天(dg,足月定义为-67 dg)结扎单侧子宫动脉。在50 dg、60 dg时,处死胎儿并将其分为生长受限(GR)组或对照组(未结扎)。对这些动物的脑组织进行固定、解剖和切片后,用NeuN抗体进行免疫组织化学分析,NeuN是大脑皮质中成熟神经元的标志物。

结果

在50 dg时,GR组和对照组大脑皮质中NeuN免疫反应性(IR)细胞数量无差异。然而,在60 dg时,GR组胎儿的NeuN-IR细胞数量少于对照组(p<0.05)。

结论

这些结果表明,产前慢性缺氧会影响60 dg时豚鼠胎儿大脑皮质中的神经元数量。本研究中使用的方法有助于扩展我们对大脑皮质神经发生的理解,这些发现可能有助于阐明产前缺氧引起的脑损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/1c907d01b2a5/jkns-56-488-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/d6f36bc9b7af/jkns-56-488-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/8c0af1da0796/jkns-56-488-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/d21cb825bebf/jkns-56-488-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/0be1a646235b/jkns-56-488-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/1c907d01b2a5/jkns-56-488-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/d6f36bc9b7af/jkns-56-488-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/8c0af1da0796/jkns-56-488-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/d21cb825bebf/jkns-56-488-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/0be1a646235b/jkns-56-488-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83d/4303724/1c907d01b2a5/jkns-56-488-g005.jpg

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本文引用的文献

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Early biochemical effects after unilateral hypoxia-ischemia in the immature rat brain.未成熟大鼠脑单侧缺氧缺血后的早期生化效应。
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The effect of hypoxia on the functional and structural development of the chick brain.缺氧对雏鸡大脑功能和结构发育的影响。
慢性产前缺氧后神经发生区Pax6的区域免疫反应性
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Hypoxia/ischemia depletes the rat perinatal subventricular zone of oligodendrocyte progenitors and neural stem cells.缺氧/缺血会使新生大鼠脑室下区的少突胶质前体细胞和神经干细胞减少。
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