PDF(Pubmed)
Abstract：
Clinical studies have found that neonatal sevoflurane exposure can increase the risk of cognitive dysfunction. However, recent studies have found that it can exhibit neuroprotective effects in some situations. In this study, we aimed to explore the effects of sevoflurane neonatal exposure in rats. A total of 144 rat pups (72 males and 72 females) were assigned to six groups and separately according to sevoflurane exposure of different times on the seventh day after birth. Blood gas analysis and western blot detection in the hippocampus were conducted after exposure. The Morris water maze test was conducted on the 32nd to 38th days after birth. The expression of PSD95 and synaptophysin in the hippocampus was detected after the Morris water maze test. We found that neonatal exposure to sevoflurane promoted apoptosis in the hippocampus, and Bax and caspase-3 were increased in a dose-dependent manner. The 2-h exposure had the greatest effects on cognitive dysfunction. However, with the extension of exposure time to 6 h, the effects on cognitive function were partly compensated. In addition, sevoflurane exposure decreased synaptogenesis in the hippocampus. However, as the exposure time was extended, the suppression of synaptogenesis was attenuated. In conclusion, neonatal sevoflurane exposure exhibited duration-dependent effects on cognitive function via Bax-caspase-3-dependent apoptosis and bidirectional effects on synaptogenesis in rats.
摘要：
临床研究发现,新生儿七氟醚暴露可增加认知功能障碍的风险。然而,最近的研究发现，它可以在某些情况下表现出神经保护作用。在这项研究中,目的探讨七氟烷暴露对新生大鼠的影响。将144只幼鼠（72只雄性和72只雌性）分为6组，分别根据出生后第7天不同时间的七氟烷暴露量。暴露后在海马中进行血气分析和蛋白质印迹检测。Morris水迷宫试验在出生后第32至38天进行。Morris水迷宫试验后检测海马中PSD95和突触素的表达。我们发现，新生儿暴露于七氟醚促进海马细胞凋亡，Bax和caspase-3呈剂量依赖性增加。2小时暴露对认知功能障碍的影响最大。然而,随着曝光时间延长至6h,对认知功能的影响得到部分补偿。此外,七氟醚暴露减少海马突触发生。然而,随着暴露时间的延长，突触发生的抑制减弱。总之,新生儿七氟醚暴露通过Bax-caspase-3依赖性细胞凋亡对认知功能有持续时间依赖性,对大鼠突触发生有双向作用.
