期刊论文详细信息
Frontiers in Psychology
Inhibited Endogenous H 2 S Generation and Excessive Autophagy in Hippocampus Contribute to Sleep Deprivation-Induced Cognitive Impairment
article
San-Qiao Yang1  Xiao-Qing Tang1  Li Jiang1  Fang Lan1  Hai-jun Wei1  Ming Xie2  Wei Zou3  Ping Zhang3  Chun-Yan Wang1  Yu-Rong Xie4 
[1] Institute of Neuroscience, Hengyang Medical College, University of South China;Department of Neurology, First Affiliated Hospital of University of South China;Department of Neurology, Affiliated Nanhua Hospital, University of South China;College of Chemistry and Chemical Engineering, University of South China
关键词: autophagy;    cognitive impairment;    hydrogen sulfide;    sleep deprivation;    hippocampus;   
DOI  :  10.3389/fpsyg.2019.00053
学科分类:社会科学、人文和艺术(综合)
来源: Frontiers
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【 摘 要 】

Background and Aim: Sleep deprivation (SD) causes deficit of cognition, but the mechanisms remain to be fully established. Hydrogen sulfide (H 2 S) plays an important role in the formation of cognition, while excessive and prolonged autophagy in hippocampus triggers cognitive disorder. In this work, we proposed that disturbances in hippocampal endogenous H 2 S generation and autophagy might be involved in SD-induced cognitive impairment. Methods: After treatment of adult male wistar rats with 72-h SD, the Y-maze test, object location test (OLT), novel object recognition test (NORT) and the Morris water maze (MWM) test were performed to determine the cognitive function. The autophagosome formation was observed with electron microscope. Generation of endogenous H 2 S in the hippocampus of rats was detected using unisense H 2 S microsensor method. The expressions of cystathionine-β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), beclin-1, light chain LC3 II/LC3 I, and p62 in the hippocampus were assessed by western blotting. Results: The Y-maze, OLT, NORT, and MWM test demonstrated that SD-exposed rats exhibited cognitive dysfunction. SD triggered the elevation of hippocampal autophagy as evidenced by enhancement of autophagosome, up-regulations of beclin-1 and LC3 II/LC3 I, and down-regulation of p62. Meanwhile, the generation of endogenous H 2 S and the expressions of CBS and 3-MST (H 2 S producing enzyme) in the hippocampus of SD-treated rats were reduced. Conclusion: These results suggested that inhibition of endogenous H 2 S generation and excessiveness of autophagy in hippocampus are involved in SD-induced cognitive impairment.

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