七氟醚通过诱导海马神经元细胞凋亡损害阿尔茨海默病转基因小鼠模型学习和记忆的功能
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Sevoflurane impairs learning and memory function in
transgenic mice model of Alzheimer’s disease by
induction of hippocampal neuron apoptosis
背景与目的
研究七氟醚对阿尔茨海默病转基因小鼠模型的学习和记忆功能的机制和作用。
方 法
总共使用 Tg2576小鼠45只，并随机分为对照组、假手术组和七氟醚组。利用莫里斯水迷宫（MWM）和y-迷宫进行行为测试，测试吸入七氟醚前后的空间学习和记忆能力。此外，为了确定海马体（CA）1、CA3和齿状回（DG）区域内的细胞凋亡，进行了TUNEL分析。使用蛋白免疫印迹法对海马中的凋亡相关蛋白（caspase-3和抗凋亡基因bcl-xL）的表达进行了分析。
结 果
MWM的结果表明，吸入七氟醚后三组在游泳速度上并没有显著的差异。然而，七氟醚组吸入七氟醚后，与假手术组和对照组（P<0.05）相比，在原象限的逃避潜伏期、时间和y-迷宫的正确反应次数减少。此外，七氟醚组CA1和CA3区域的凋亡细胞数明显高于假手术组和对照组（P<0.05）。蛋白免疫印迹法结果表明，Bcl-xL的蛋白质表达水平明显更高，但在七氟醚组中，caspase-3水平明显低于对照组和假手术组（P<0.05）。
结 论
我们的研究结果表明，七氟醚可能会通过诱导AD小鼠模型海马神经元细胞凋亡来损害学习和记忆功能。
原始文献摘要
Jia Z, Geng L, Xie G, et al. Sevoflurane impairs acquisition learning and memory function in transgenic mice model of Alzheimer’s disease by induction of hippocampal neuron apoptosis[J]. Int J Clin Exp Med, 2015, 8(9):15490-15497.
Objectives: To investigate the mechanism and effect of sevoflurane on learning and memory function in transgenic mice model of Alzheimer s disease (AD).
Methods: A total of 45 Tg2576 mice were used and randomly assigned to control, sham, and sevoflurane group. Spatial learning and memory ability were measured before and after sevoflurane exposure using morris water maze (MWM) and Y-maze behavioral tests. Moreover, TUNEL assay was carried out to determine the cell death in hippocampal cornuammonis (CA) 1, CA3, and dentate gyrus (DG) region. Apoptosis-related protein (caspase-3 and Bcl-xL) expression in the hippocampus was analyzed by Western blotting.
Results: The MWM results showed that there were no significant differences in the swimming speed after sevoflurane exposure among the three groups. However, the escape latency, time spent in original quadrant, and the number of correct trials (Y-maze) were significantly lower after sevoflurane anesthesia exposure in the sevoflurane group than the sham group and control group (P < 0.05). Besides, the apoptotic cell numbers of the CA1 and CA3 region in the sevoflurane group were significantly higher than those in the sham group and control group (P < 0.05). Western blotting results showed that the protein expression levels of Bcl-xL were significantly higher, but the caspase-3 levels were significantly lower in the sevoflurane group than those in the control group and sham group (both P < 0.05).
Conclusion: Our results indicate that sevoflurane might impair acquisition learning and memory function in AD by induction of hippocampal neuron apoptosis.
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