Increasing evidence indicates that exposure to inflammation during pregnancy intensifies the offspring’s cognitive impairment during aging, which might be correlated with changes in some synaptic plasticity-related proteins. In addition, an enriched environment (EE) can significantly exert a beneficial impact on cognition and synaptic plasticity. However, it is unclear whether gestational inflammation combined with postnatal EE affects the changes in cognition and synaptic plasticity-related proteins during aging. In this study, pregnant mice were intraperitoneally injected with lipopolysaccharides (LPS, 50 μg/kg) or normal saline at days 15–17 of pregnancy. At 21 days after delivery, some LPS-treated mice were randomly selected for EE treatment. At the age of 6 and 18 months, Morris water maze (MWM) and western blotting were, respectively, used to evaluate or measure the ability of spatial learning and memory and the levels of postsynaptic plasticity-related proteins in the hippocampus, including postsynaptic density protein 95 (PSD-95), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) GluA1 subunit, and Homer-1b/c. The results showed that 18-month-old control mice had worse spatial learning and memory and lower levels of these synaptic plasticity-related proteins (PSD-95, GluA1, and Homer-1b/c) than the 6-month-old controls. Gestational LPS exposure exacerbated these age-related changes of cognition and synaptic proteins, but EE could alleviate the treatment effect of LPS. In addition, the performance during learning and memory periods in the MWM correlated with the hippocampal levels of PSD-95, GluA1, and Homer-1b/c. Our results suggested that gestational inflammation accelerated age-related cognitive impairment and the decline of PSD-95, GluA1, and Homer-1b/c protein expression, and postpartum EE could alleviate these changes.

中文翻译：

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产后丰富环境对妊娠期炎症的影响与年龄相关的认知和海马突触可塑性相关蛋白的变化

越来越多的证据表明，怀孕期间暴露于炎症会加剧衰老过程中后代的认知障碍，这可能与某些突触可塑性相关蛋白的变化有关。此外，丰富的环境（EE）可以对认知和突触可塑性产生显着的有益影响。然而，尚不清楚妊娠炎症与产后EE结合是否会影响衰老过程中认知和突触可塑性相关蛋白的变化。在这项研究中，孕小鼠腹膜内注射脂多糖（LPS，50  μ孕15–17天时服用生理盐水）。分娩后21天，随机选择一些接受LPS治疗的小鼠进行EE治疗。在6和18个月大时，分别使用莫里斯水迷宫（MWM）和蛋白质印迹法评估或测量空间学习和记忆的能力以及海马中突触后可塑性相关蛋白的水平，包括突触后密度。蛋白质95（PSD-95），α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（AMPAR）GluA1亚基和Homer-1b / c。结果显示，与6个月大的对照组相比，18个月大的对照组小鼠的学习和记忆能力较差，这些突触可塑性相关蛋白（PSD-95，GluA1和Homer-1b / c）的水平较低。妊娠LPS暴露加剧了这些年龄相关的认知和突触蛋白的变化，但是EE可以减轻LPS的治疗效果。另外，MWM在学习和记忆期间的表现与PSD-95，GluA1和Homer-1b / c的海马水平相关。我们的研究结果表明，妊娠炎症会加速与年龄有关的认知障碍，PSD-95，GluA1和Homer-1b / c蛋白表达下降，而产后EE可以缓解这些变化。