首页> 美国卫生研究院文献>Journal of Neuroinflammation >Enhanced neuroinflammation mediated by DNA methylation of the glucocorticoid receptor triggers cognitive dysfunction after sevoflurane anesthesia in adult rats subjected to maternal separation during the neonatal period
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Enhanced neuroinflammation mediated by DNA methylation of the glucocorticoid receptor triggers cognitive dysfunction after sevoflurane anesthesia in adult rats subjected to maternal separation during the neonatal period

机译:七氟醚麻醉后成年大鼠在新生儿期接受母体分离后糖皮质激素受体的DNA甲基化介导的神经炎症增强引发认知功能障碍

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摘要

BackgroundMounting evidence indicates that children who experience abuse and neglect are prone to chronic diseases and premature mortality later in life. One mechanistic hypothesis for this phenomenon is that early life adversity alters the expression or functioning of the glucocorticoid receptor (GR) throughout the course of life and thereby increases sensitivity to inflammatory stimulation. An exaggerated pro-inflammatory response is generally considered to be a key cause of postoperative cognitive dysfunction (POCD). The aim of this study was to examine the effects of early life adversity on cognitive function and neuroinflammation after sevoflurane anesthesia in adult rats and to determine whether such effects are associated with the epigenetic regulation of GR.
机译:背景技术有证据表明,遭受虐待和忽视的儿童在以后的生活中容易患慢性疾病和过早死亡。这种现象的一种机械学说是,生命的早期逆境会改变整个生命过程中糖皮质激素受体(GR)的表达或功能,从而增加对炎症刺激的敏感性。一般认为,过度的促炎反应是术后认知功能障碍(POCD)的关键原因。这项研究的目的是检查七氟醚麻醉后成年大鼠早期逆境对认知功能和神经炎症的影响,并确定这种影响是否与GR的表观遗传调控有关。

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