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首页> 外文期刊>Scientific reports. >Administration of molecular hydrogen during pregnancy improves behavioral abnormalities of offspring in a maternal immune activation model
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Administration of molecular hydrogen during pregnancy improves behavioral abnormalities of offspring in a maternal immune activation model

机译：怀孕期间给予氢分子可改善母体免疫激活模型中后代的行为异常

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The aim of the present study was to investigate long-term outcomes of the offspring in a lipopolysaccharide (LPS)-induced maternal immune activation (MIA) model and the effect of maternal molecular hydrogen (H2) administration. We have previously demonstrated in the MIA mouse model that maternal administration of H2 attenuates oxidative damage and neuroinflammation, including induced pro-inflammatory cytokines and microglial activation, in the fetal brain. Short-term memory, sociability and social novelty, and sensorimotor gating were evaluated using the Y-maze, three-chamber, and prepulse inhibition (PPI) tests, respectively, at postnatal 3 or 4 weeks. The number of neurons and oligodendrocytes was also analyzed at postnatal 5 weeks by immunohistochemical analysis. Offspring of the LPS-exposed dams showed deficits in short-term memory and social interaction, following neuronal and oligodendrocytic loss in the amygdala and cortex. Maternal H2 administration markedly attenuated these LPS-induced abnormalities. Moreover, we evaluated the effect of H2 on LPS-induced astrocytic activation, both in vivo and in vitro. The number of activated astrocytes with hypertrophic morphology was increased in LPS-exposed offspring, but decreased in the offspring of H2-administered dams. In primary cultured astrocytes, LPS-induced pro-inflammatory cytokines were attenuated by H2 administration. Overall, these findings indicate that maternal H2 administration exerts neuroprotective effects and ameliorates MIA-induced neurodevelopmental deficits of offspring later in life.
机译：本研究的目的是研究脂多糖（LPS）诱导的母体免疫激活（MIA）模型中后代的长期结果以及母体分子氢（H2）施用的影响。我们先前在MIA小鼠模型中证明，母体给予H2可以减轻胎儿脑中的氧化损伤和神经炎症，包括诱导的促炎性细胞因子和小胶质细胞活化。在出生后3周或4周分别使用Y迷宫，三腔室和脉冲前抑制（PPI）测试来评估短期记忆，社交能力和社交新颖性，以及感觉运动门控。还通过免疫组织化学分析在出生后5周分析神经元和少突胶质细胞的数量。 LPS暴露的水坝的后代在杏仁核和皮层神经元和少突胶质细胞丧失后，显示出短期记忆和社交互动不足。孕妇注射H2可以显着减轻LPS诱发的这些异常。此外，我们评估了H2在体内和体外对LPS诱导的星形细胞活化的影响。暴露于LPS的后代中，具有肥大形态的活化星形胶质细胞数量增加，但在H2施用的大坝的后代中，数量减少。在原代培养的星形胶质细胞中，LPS诱导的促炎细胞因子通过H2给药而减弱。总体而言，这些发现表明，母亲给予H2可以发挥神经保护作用，并减轻MIA诱导的后代后代神经发育缺陷。

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