Effects of Antenatal Steroid Therapy on Neurodevelopment in an IUGR Mouse Model
Effects of Antenatal Steroid Therapy on Neurodevelopment in an IUGR Mouse Model
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产前类固醇治疗对 IUGR 小鼠模型神经发育的影响
DOI：
10.1159/000316102
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发表时间：
2010
影响因子：
2.2
通讯作者：
Y. Kimura
中科院分区：
文献类型：
--
作者：
C. Velayo;Takuya Ito;H. Chisaka;N. Yaegashi;K. Okamura;Y. Kimura
背景/目的：研究产后小鼠对产前类固醇治疗与母体蛋白限制相关的神经发育反应。方法：C57BL/6N妊娠小鼠（n = 24，每个治疗组4只）给予对照(C)或蛋白限制（PR）饮食，并在妊娠后期（E10-E17）每日皮下注射100 μ l/kg的地塞米松磷酸钠与生理盐水（C- d /S, PR- d /S）或单独的生理盐水（C-S, PR-S）。非治疗组也包括在内（C， PR）。在出生后第7天采集幼崽脑样本，采用免疫组织化学和qRT-PCR分析。结果：各治疗组新生儿体重均小于C组，但脑容量差异无统计学意义。神经胶质细胞的免疫组织化学评价显示，蛋白质限制对少突胶质细胞和少突胶质前体细胞有明显的影响，胎儿对应激和地塞米松有不同的反应。利用定量RNA分析的进一步评估显示，PR-D/S组Galr1、Galr2、Igfbp-1、Igfbp-3、Igfbp-6和Fgf2的激活显著增加了1- 2.5倍，PR-S组的激活幅度更高，为1- 10.5倍。结论：本初步研究揭示了地塞米松在进一步增加损伤易感神经胶质细胞的细胞损伤易感性中的可能作用。关键胶质标记物的分布和几种神经营养因子的过度表达描述了持续的细胞适应。
Background/Objective: To investigate the neurodevelopmental response in postnatal mice secondary to antenatal steroid treatment in association with maternal protein restriction. Methods: C57BL/6N pregnant mice (n = 24; 4 per treatment group) were administered control (C) or protein-restricted (PR) diets and subjected to daily subcutaneous injection stress during late gestation (E10–E17) with either 100 µl/kg of dexamethasone sodium phosphate in normosaline (C-D/S, PR-D/S) or normosaline alone (C-S, PR-S). Non-treatment groups were also included (C, PR). Brain samples of pups were collected on postnatal day 7 and analyzed by immunohistochemistry and qRT-PCR. Results: Neonatal weights in the treatment groups were smaller than their counterparts in the C group, but there were no significant differences in brain size. Immunohistochemical evaluation of neuroglial cells revealed a pronounced effect of protein restriction on oligodendrocytes and oligodendrocyte precursor cells with distinct fetal responses to stress and dexamethasone. Further evaluation using quantitative RNA analysis showed significant activation of Galr1, Galr2, Igfbp-1, Igfbp-3, Igfbp-6, and Fgf2 by 1- to 2.5-fold in the PR-D/S group and by much higher increments, 1- to 10.5-fold, in the PR-S group. Conclusion: This preliminary investigation revealed the possible role of dexamethasone in further increasing vulnerability to cell damage in injury-prone neuroglial cells. The distribution of key glial markers and the overexpression of several neurotrophic factors depicted ongoing cellular adaptation.
DOI：
10.1073/pnas.0506375102
发表时间：
2005-12-13
影响因子：
11.1
作者：
Jin, KL;LaFevre-Bernt, M;Ellerby, LM
通讯作者：
Ellerby, LM