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// Xiao-Na Li 1, 2, * , Lei Chen 1, 3, * , Bang Luo 1, 4, * , Xiang Li 1, 5 , Chun-Yan Wang 1, 6 , Wei Zou 1, 3 , Ping Zhang 1, 3 , Yong You 1, 4 and Xiao-Qing Tang 1, 2 1 Institute 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 2 Department of Physiology, Medical College, University of South China, Hengyang 421001, Hunan, P. R. China 3 Department of Neurology, Nanhua Affiliated Hospital, University of South China, Hengyang 421001, Hunan, P. R. China 4 Department of Neurology, The First Affiliated Hospital, University of South China, Hengyang 421001, Hunan, P. R. China 5 Department of Anaesthesiology, The First Affiliated Hospital, University of South China, Hengyang 421001, Hunan, P. R. China 6 Department 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: tangxq-usc@qq.com , tangxq-usc@usc.edu.cn Wei Zou, email: zouw415@163.com 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 (H 2 S), 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 H 2 S 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 H 2 S) 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 H 2 S meliorates CRS-induced hippocampal damage and cognitive impairment by upregulation of hippocampal Sirt1.
Li et al. (Wed,) studied this question.