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术后24小时急性睡眠剥夺通过抑制脾切除大鼠海马神经元中tau蛋白磷酸化改善学习和记忆。

Postoperative 24-h Acute Sleep Deprivation Improves Learning and Memory Through Inhibition of Tau Phosphorylation in the Hippocampal Neurons of Splenectomized Rats.

作者信息

Zhang Yu-Wei, Li Xiao-Qian, Tan Wen-Fei, Fang Bo, Ma Hong

机构信息

Department of Anesthesiology, The First Hospital of China Medical University, Shenyang, People's Republic of China.

Department of Anesthesiology, The First Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.

出版信息

Nat Sci Sleep. 2020 Aug 24;12:603-613. doi: 10.2147/NSS.S254449. eCollection 2020.

Abstract

PURPOSE

As tau pathology is involved in impaired postoperative learning and memory in rats, we attempted to identify the possible mechanisms by which tau pathology affects postoperative sleep deprivation.

METHODS

Adult male Sprague-Dawley rats were randomly assigned into six groups as follows: the Control group, Anaesthesia group, Surgery group, Sleep deprivation (SD) group: 24-h SD with the modified multiple platform method (MMPM), Anaesthesia and SD (ASD) group, and Surgery and SD (SSD) group. Tau396 and FOXQ1 protein expression levels in the hippocampal neurons of all groups were analysed. Changes following co-culture of hippocampal neurons with IL-6 were detected by flow cytometry.

RESULTS

Twenty-four hours of acute SD decreased the error scores on postoperative day 5 in the ASD and SSD groups compared with the Anaesthesia and Surgery groups. Compared with the tau levels in the Control group, tau levels in the Anaesthesia and Surgery groups were increased, but SD decreased the expression of tau in the ASD and SSD groups. The expression levels of tau and FOXQ1 were inversely regulated. When hippocampal neurons were co-cultured with IL-6, the same changes were observed.

CONCLUSION

Postoperative 24-h acute SD improves learning and memory through inhibition of tau phosphorylation and increases IL-6-induced expression of FOXQ1 in the hippocampal neurons of splenectomized rats.

摘要

目的

由于tau病理改变与大鼠术后学习记忆受损有关,我们试图确定tau病理影响术后睡眠剥夺的可能机制。

方法

将成年雄性Sprague-Dawley大鼠随机分为六组:对照组、麻醉组、手术组、睡眠剥夺(SD)组:采用改良多平台法(MMPM)进行24小时睡眠剥夺、麻醉与睡眠剥夺(ASD)组、手术与睡眠剥夺(SSD)组。分析所有组海马神经元中Tau396和FOXQ1蛋白表达水平。通过流式细胞术检测海马神经元与IL-6共培养后的变化。

结果

与麻醉组和手术组相比,24小时急性睡眠剥夺降低了ASD组和SSD组术后第5天的错误评分。与对照组的tau水平相比,麻醉组和手术组的tau水平升高,但睡眠剥夺降低了ASD组和SSD组中tau的表达。tau和FOXQ1的表达水平呈负调控。当海马神经元与IL-6共培养时,观察到相同的变化。

结论

术后24小时急性睡眠剥夺通过抑制tau磷酸化改善学习记忆,并增加IL-6诱导的脾切除大鼠海马神经元中FOXQ1的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b80/7455769/0c6b33a6d72a/NSS-12-603-g0001.jpg

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