Hydrogen Sulfide Prevents Sleep Deprivation-Induced Hippocampal Damage by Upregulation of Sirt1 in the Hippocampus

Jin-Xi Zuo; Min Li; Li Jiang; Fang Lan; Yi-Yun Tang; Xuan Kang; Wei Zou; Chun-Yan Wang; Ping Zhang; Xiao-Qing Tang

doi:10.3389/fnins.2020.00169

Hydrogen Sulfide Prevents Sleep Deprivation-Induced Hippocampal Damage by Upregulation of Sirt1 in the Hippocampus

Front Neurosci. 2020 Mar 11:14:169. doi: 10.3389/fnins.2020.00169. eCollection 2020.

Authors

Jin-Xi Zuo¹, Min Li¹, Li Jiang¹, Fang Lan^{2

3}, Yi-Yun Tang⁴, Xuan Kang^{3

4}, Wei Zou¹, Chun-Yan Wang⁴, Ping Zhang¹, Xiao-Qing Tang^{3

4}

Affiliations

¹ Department of Neurology, Affiliated Nanhua Hospital, University of South China, Hengyang, China.
² Department of Neurology, The First Affiliated Hospital, University of South China, Hengyang, China.
³ Institute of Neurology, The First Affiliated Hospital, University of South China, Hengyang, China.
⁴ Department of Physiology, Hengyang Medical College, University of South China, Hengyang, China.

Abstract

Sleep deprivation (SD) induces hippocampal damage. Hydrogen sulfide (H₂S) is a neuronal protective factor. Silence information regulating factor 1 (Sirt1) plays an important role in neuroprotection. Therefore, this study was aimed at exploring whether H₂S meliorates SD-induced hippocampal damage and whether Sirt1 mediates this protective role of H₂S. We found that sodium hydrosulfide (NaHS, a donor of H₂S) alleviated SD-generated hippocampal oxidative stress, including increases in the activation of SOD and the level of GSH as well as a decrease in the level of MDA. Meanwhile, we found that NaHS reduced SD-exerted hippocampal endoplasmic reticulum (ER) Stress, including downregulations of GRP78, CHOP, and cleaved-caspase-12 expression. Moreover, NaHS reduced the apoptosis in the SD-exposed hippocampus, and this included decreases in the number of apoptotic cells and the activation of caspase-3, downregulation of Bax expression, and upregulation of Bcl-2 expression. NaHS upregulated the expression of Sirt1 in the hippocampus of SD-exposed rats. Furthermore, Sirtinol, the inhibitor of Sirt1, abrogated the protection of NaHS against SD-exerted hippocampal oxidative stress, ER stress, and apoptosis. These results suggested that H₂S alleviates SD-induced hippocampal damage by upregulation of hippocampal Sirt1.

Keywords: hippocampal damage; hydrogen sulfide; oxidative stress; silence information regulating factor 1; sleep deprivation.