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电针预处理可改善大鼠高空超重诱导的学习记忆损伤和海马神经元凋亡。

Electroacupuncture pretreatment ameliorates hypergravity-induced impairment of learning and memory and apoptosis of hippocampal neurons in rats.

机构信息

Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, China.

出版信息

Neurosci Lett. 2010 Jul 12;478(3):150-5. doi: 10.1016/j.neulet.2010.05.006. Epub 2010 May 10.

DOI:10.1016/j.neulet.2010.05.006
PMID:20457216
Abstract

High-sustained positive acceleration (+Gz) exposures might lead to impairment in cognitive function. Our previous studies have shown that electroacupuncture (EA) pretreatment can attenuate transient focal cerebral ischemic injury in the rats. In this study we aimed to investigate whether EA pretreatment could ameliorate the impairment of learning and memory induced by a sustained +Gz exposure. Using the centrifuge model, rats of experimental groups were exposed to +10 Gz for 5 min. Morris water maze was used for assessing the cognitive ability, and the apoptotic hippocampal CA1 pyramidal neuronal cells were evaluated by caspase-3 activity and TUNEL staining. Our results showed that +Gz exposure significantly caused pyramidal neuronal damage, increased neuronal apoptosis and caspase-3 activity in hippocampal CA1 region, as well as resulted in an impairment of spatial learning and memory, as compared to the sham group animals. Furthermore, the EA pretreatment significantly attenuated the neuronal apoptosis, preserved neuronal morphology and inhibited the caspase-3 activity in hippocampal CA1 region resulted from +Gz exposure. The EA pretreatment also ameliorated the learning and memory function in rats exposed to +Gz. These findings indicate that EA pretreatment provides a novel method to prevent the cognitive damage caused by +Gz, which could significantly protect neuronal damage and impairment of learning and memory.

摘要

高持续正加速度(+Gz)暴露可能导致认知功能障碍。我们之前的研究表明,电针(EA)预处理可以减轻大鼠短暂性局灶性脑缺血损伤。在这项研究中,我们旨在研究 EA 预处理是否可以改善持续+Gz 暴露引起的学习和记忆损伤。使用离心机模型,实验组大鼠暴露于+10 Gz 持续 5 分钟。Morris 水迷宫用于评估认知能力,通过 caspase-3 活性和 TUNEL 染色评估海马 CA1 区的凋亡锥体神经元细胞。我们的结果表明,与假手术组动物相比,+Gz 暴露会导致锥体神经元损伤、海马 CA1 区神经元凋亡和 caspase-3 活性增加,并导致空间学习和记忆损伤。此外,EA 预处理可显著减轻+Gz 暴露引起的海马 CA1 区神经元凋亡、保持神经元形态和抑制 caspase-3 活性。EA 预处理还改善了暴露于+Gz 的大鼠的学习和记忆功能。这些发现表明,EA 预处理为预防+Gz 引起的认知损伤提供了一种新方法,可显著保护神经元损伤和学习记忆损伤。

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