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Front. Behav. Neurosci. | doi: 10.3389/fnbeh.2019.00244

Hydrogen sulfide attenuates β2-microglobulin-induced cognitive dysfunction: involving recovery of hippocampal autophagic flux

 Si-Min Chen1, Yi-Li Yi2,  Dan Zeng2, Yi-Yun Tang3, Xuan Kang1, 3,  Wei Zou2, 3* and  Xiao-Qing Tang1, 3, 4*
  • 1Department of Neurology, the First Affiliated Hospital, University of South China, China
  • 2Department of Neurology, the Affiliated Nanhua Hospital, University of South China, China
  • 3Institute of Neuroscience, Hengyang Medical College, University of South China, China
  • 4University of South China, China

Background and Aim: Accumulation of β2-microglobulin (B2M), a systemic pro-aging factor, regulates negatively cognitive function. Hydrogen sulfide (H2S), a novel gas signaling molecule, exerts protection against cognitive dysfunction. Therefore, the present work was designed to explore whether H2S attenuates cognitive dysfunction induced by B2M and its underlying mechanism.
Materials and Methods: The cognitive function of rats was assessed by Y-maze, Novel object recognition (NOR), and Morris water maze (MWM) tests. The levels of autophagosome and autolysosome in hippocampus were observed by transmission electron microscopy. The expression of p62 protein in hippocampus was detected by western blot analysis.
Results: NaHS (a donor of H2S) significantly alleviated cognitive impairments in the B2M-exposed rats tested by Y-maze test, NOR test and MWM test. Furthermore, NaHS recovered autophagic flux in the hippocampus of B2M-exposed rats, as evidenced by decreases in the ratio of autophagosome to autolysosome and the expression of p62 protein in the hippocampus.
Conclusion: In summary, these data indicated that H2S attenuates B2M-induced cognitive dysfunction, involving in recovery of the blocked autophagic flux in the hippocampus, and suggested that H2S may be a novel approach to prevent B2M-induced cognitive dysfunction.

Keywords: Hydrogen Sulfide, β2-microglobulin, cognitive dysfunction, Autophagic Flux, Hippocampus

Received: 25 Jul 2019; Accepted: 04 Oct 2019.

Copyright: © 2019 Chen, Yi, Zeng, Tang, Kang, Zou and Tang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Prof. Wei Zou, Department of Neurology, the Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan, China,
Prof. Xiao-Qing Tang, University of South China, Hengyang, China,