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丙泊酚通过抑制线粒体自噬和自噬来保护睡眠剥夺大鼠的海马神经元。

Propofol protects hippocampal neurons in sleep-deprived rats by inhibiting mitophagy and autophagy.

作者信息

Dai Weixin, Xiao Yong, Tu Youbing, Xiao Fei, Lu Yizhi, Qin Yinying, Xie Yubo

机构信息

Department of Anesthesiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.

出版信息

Ann Transl Med. 2021 Sep;9(18):1427. doi: 10.21037/atm-21-3872.

DOI:10.21037/atm-21-3872
PMID:34733979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8506745/
Abstract

BACKGROUND

Sleep deprivation (SD) causes a disturbance in the cognitive function of rats. While propofol has a powerful sedative and hypnotic effect and is an antioxidant, its effect on the cognitive function of rats following SD remains unknown. The purpose of this study was to explore the protective effects of propofol on excessive autophagy and mitophagy in the hippocampus of rats after SD.

METHODS

Adult male rats were intraperitoneally injected with 30 mg/kg of propofol after 96 hours of SD. Then we evaluated the effect of propofol on the cognitive function of sleep deprived rats by the Morris water maze. Transmission electron microscopy, Western blotting, PCR, immunohistochemistry, autophagy enhancer and autophagy inhibitor were used to study the effect of propofol on hippocampal neurons of rat with excessive autophagy and mitophagy.

RESULTS

The behavioral experimental results of the Morris water maze showed that propofol improved the learning and memory ability of sleep-deprived rats. The expression of Beclin1, PINK1, parkin, p62, and LC3 protein increased significantly after sleep deprivation. While the intervention of propofol could significantly reduce the expression of these proteins, rapamycin treatment eliminated this effect.

CONCLUSIONS

Our findings showed that propofol could reduce the impairment of learning and memory in sleep-deprived rats by inhibiting excessive autophagy and mitophagy in hippocampal neurons. This strategy may provide an application basis for the clinical use of propofol in patients with chronic insomnia.

摘要

背景

睡眠剥夺（SD）会导致大鼠认知功能紊乱。虽然丙泊酚具有强大的镇静催眠作用且是一种抗氧化剂，但其对睡眠剥夺后大鼠认知功能的影响尚不清楚。本研究的目的是探讨丙泊酚对睡眠剥夺后大鼠海马体过度自噬和线粒体自噬的保护作用。

方法

成年雄性大鼠在睡眠剥夺96小时后腹腔注射30mg/kg丙泊酚。然后通过莫里斯水迷宫评估丙泊酚对睡眠剥夺大鼠认知功能的影响。采用透射电子显微镜、蛋白质免疫印迹法、聚合酶链反应、免疫组织化学、自噬增强剂和自噬抑制剂研究丙泊酚对自噬和线粒体自噬过度的大鼠海马神经元的影响。

结果

莫里斯水迷宫行为实验结果表明，丙泊酚改善了睡眠剥夺大鼠的学习和记忆能力。睡眠剥夺后，Beclin1、PINK1、parkin、p62和LC3蛋白的表达显著增加。而丙泊酚干预可显著降低这些蛋白的表达，雷帕霉素处理消除了这种作用。

结论

我们的研究结果表明，丙泊酚可通过抑制海马神经元过度自噬和线粒体自噬来减轻睡眠剥夺大鼠的学习和记忆损伤。该策略可能为丙泊酚在慢性失眠患者临床应用中提供应用依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/d751d7977bf2/atm-09-18-1427-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/12d0b90ecf5f/atm-09-18-1427-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/ffb9e66d3cb4/atm-09-18-1427-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/2a30364f4629/atm-09-18-1427-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/7c55ff734b59/atm-09-18-1427-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/6742a21aa00c/atm-09-18-1427-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/d751d7977bf2/atm-09-18-1427-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/12d0b90ecf5f/atm-09-18-1427-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/ffb9e66d3cb4/atm-09-18-1427-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/2a30364f4629/atm-09-18-1427-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/7c55ff734b59/atm-09-18-1427-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/6742a21aa00c/atm-09-18-1427-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc69/8506745/d751d7977bf2/atm-09-18-1427-f6.jpg

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