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Hydrogen Sulfide Attenuates β2-Microglobulin-Induced Cognitive Dysfunction: Involving Recovery of Hippocampal Autophagic Flux
BACKGROUND AND AIM: Accumulation of β(2)-microglobulin (B2M), a systemic pro-aging factor, regulates negatively cognitive function. Hydrogen sulfide (H(2)S), a novel gas signaling molecule, exerts protection against cognitive dysfunction. Therefore, the present work was designed to explore whether H...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823620/ https://www.ncbi.nlm.nih.gov/pubmed/31708756 http://dx.doi.org/10.3389/fnbeh.2019.00244 |
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author | Chen, Si-Min Yi, Yi-Li Zeng, Dan Tang, Yi-Yun Kang, Xuan Zhang, Ping Zou, Wei Tang, Xiao-Qing |
author_facet | Chen, Si-Min Yi, Yi-Li Zeng, Dan Tang, Yi-Yun Kang, Xuan Zhang, Ping Zou, Wei Tang, Xiao-Qing |
author_sort | Chen, Si-Min |
collection | PubMed |
description | BACKGROUND AND AIM: Accumulation of β(2)-microglobulin (B2M), a systemic pro-aging factor, regulates negatively cognitive function. Hydrogen sulfide (H(2)S), a novel gas signaling molecule, exerts protection against cognitive dysfunction. Therefore, the present work was designed to explore whether H(2)S attenuates cognitive dysfunction induced by B2M and the 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 H(2)S) 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 H(2)S attenuates B2M-induced cognitive dysfunction, involving in recovery of the blocked autophagic flux in the hippocampus, and suggested that H(2)S may be a novel approach to prevent B2M-induced cognitive dysfunction. |
format | Online Article Text |
id | pubmed-6823620 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68236202019-11-08 Hydrogen Sulfide Attenuates β2-Microglobulin-Induced Cognitive Dysfunction: Involving Recovery of Hippocampal Autophagic Flux Chen, Si-Min Yi, Yi-Li Zeng, Dan Tang, Yi-Yun Kang, Xuan Zhang, Ping Zou, Wei Tang, Xiao-Qing Front Behav Neurosci Neuroscience BACKGROUND AND AIM: Accumulation of β(2)-microglobulin (B2M), a systemic pro-aging factor, regulates negatively cognitive function. Hydrogen sulfide (H(2)S), a novel gas signaling molecule, exerts protection against cognitive dysfunction. Therefore, the present work was designed to explore whether H(2)S attenuates cognitive dysfunction induced by B2M and the 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 H(2)S) 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 H(2)S attenuates B2M-induced cognitive dysfunction, involving in recovery of the blocked autophagic flux in the hippocampus, and suggested that H(2)S may be a novel approach to prevent B2M-induced cognitive dysfunction. Frontiers Media S.A. 2019-10-25 /pmc/articles/PMC6823620/ /pubmed/31708756 http://dx.doi.org/10.3389/fnbeh.2019.00244 Text en Copyright © 2019 Chen, Yi, Zeng, Tang, Kang, Zhang, Zou and Tang. http://creativecommons.org/licenses/by/4.0/ 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. |
spellingShingle | Neuroscience Chen, Si-Min Yi, Yi-Li Zeng, Dan Tang, Yi-Yun Kang, Xuan Zhang, Ping Zou, Wei Tang, Xiao-Qing Hydrogen Sulfide Attenuates β2-Microglobulin-Induced Cognitive Dysfunction: Involving Recovery of Hippocampal Autophagic Flux |
title | Hydrogen Sulfide Attenuates β2-Microglobulin-Induced Cognitive Dysfunction: Involving Recovery of Hippocampal Autophagic Flux |
title_full | Hydrogen Sulfide Attenuates β2-Microglobulin-Induced Cognitive Dysfunction: Involving Recovery of Hippocampal Autophagic Flux |
title_fullStr | Hydrogen Sulfide Attenuates β2-Microglobulin-Induced Cognitive Dysfunction: Involving Recovery of Hippocampal Autophagic Flux |
title_full_unstemmed | Hydrogen Sulfide Attenuates β2-Microglobulin-Induced Cognitive Dysfunction: Involving Recovery of Hippocampal Autophagic Flux |
title_short | Hydrogen Sulfide Attenuates β2-Microglobulin-Induced Cognitive Dysfunction: Involving Recovery of Hippocampal Autophagic Flux |
title_sort | hydrogen sulfide attenuates β2-microglobulin-induced cognitive dysfunction: involving recovery of hippocampal autophagic flux |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823620/ https://www.ncbi.nlm.nih.gov/pubmed/31708756 http://dx.doi.org/10.3389/fnbeh.2019.00244 |
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