Research Papers:
Hydrogen sulfide attenuates chronic restrain stress-induced cognitive impairment by upreglulation of Sirt1 in hippocampus
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Abstract
Xiao-Na Li1,2,*, Lei Chen1,3,*, Bang Luo1,4,*, Xiang Li1,5, Chun-Yan Wang1,6, Wei Zou1,3, Ping Zhang1,3, Yong You1,4 and Xiao-Qing Tang1,2
1Institute of Neuroscience, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Medical College, University of South China, Hengyang 421001, Hunan, P. R. China
2Department of Physiology, Medical College, University of South China, Hengyang 421001, Hunan, P. R. China
3Department of Neurology, Nanhua Affiliated Hospital, University of South China, Hengyang 421001, Hunan, P. R. China
4Department of Neurology, The First Affiliated Hospital, University of South China, Hengyang 421001, Hunan, P. R. China
5Department of Anaesthesiology, The First Affiliated Hospital, University of South China, Hengyang 421001, Hunan, P. R. China
6Department of Pathophysiology, Medical College, University of South China, Hengyang 421001, Hunan, P. R. China
*These authors have contributed equally to this work
Correspondence to:
Xiao-Qing Tang, email: [email protected], [email protected]
Wei Zou, email: [email protected]
Keywords: cognitive impairment; chronic-restrain-stress; hydrogen sulfide; hippocampal damage; silence information regulator-1
Received: August 14, 2017 Accepted: October 05, 2017 Published: November 01, 2017
ABSTRACT
Chronic restraint stress (CRS) has detrimental effects on cognitive function. Hydrogen sulfide (H2S), as a neuromodulator, regulates learning and memory. Hippocampus is a key structure in learning and memory. Sirt1 (silence signal regulating factor 1) plays an important role in modulating cognitive function. Therefore, our present work was to investigate whether H2S meliorates CRS-induced damage in hippocampus and impairment in cognition, and further to explore whether the underlying mechanism is via upreglulating Sirt1. In our present work, the behavior experiments [Y-maze test, Novel object recognition (NOR) test, Morris water maze (MWM) test] showed that sodium hydrosulfide (NaHS, a donor of H2S) blocked CRS-induced cognitive impairments in rats. NaHS inhibited CRS-induced hippocampal oxidative stress as evidenced by decrease in MDA level as well as increases in GSH content and SOD activity. NaHS rescued CRS-generated ER stress as evidenced by downregulations of CPR78, CHOP, and cleaved caspase-12. NaHS reduced CRS-exerted apoptosis as evidenced by decreases in the number of TUNEL-positive cells and Bax expression as well as increase in Bcl-2 expression. NaHS upregulated the expression of Sirt1 in the hippocampus of CRS-exposed rats. Furthermore, inhibited Sirt1 by Sirtinol reversed the protective effects of NaHS against CRS-produced cognitive dysfunction and oxidative stress, ER stress as well as apoptosis in hippocampus. Together, these results suggest that H2S meliorates CRS-induced hippocampal damage and cognitive impairment by upregulation of hippocampal Sirt1.
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