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Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer’s Disease
BACKGROUND: In recent years, schisandrin (SCH) was proved to improve Alzheimer's Disease (AD). The aim of our study is to explore the effect of SCH on neuronal pyroptosis in the disease. METHODS: A Morris water maze test was performed to evaluate the spatial learning and memory retention of AD...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7853410/ https://www.ncbi.nlm.nih.gov/pubmed/33542629 http://dx.doi.org/10.2147/NDT.S279147 |
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author | Li, Quan Wang, Qi Guan, Huibo Zhou, Yanyan Liu, Li |
author_facet | Li, Quan Wang, Qi Guan, Huibo Zhou, Yanyan Liu, Li |
author_sort | Li, Quan |
collection | PubMed |
description | BACKGROUND: In recent years, schisandrin (SCH) was proved to improve Alzheimer's Disease (AD). The aim of our study is to explore the effect of SCH on neuronal pyroptosis in the disease. METHODS: A Morris water maze test was performed to evaluate the spatial learning and memory retention of AD mouse. ELISA was fulfilled to examine the concentration of Aβ, IL-1β, and IL-18. Western blot was performed to detect the expression of apoptosis- and pyroptosis-related proteins. Besides, the neuronal apoptosis rate was examined using TUNEL assay. Immunohistochemistry was utilized to detect the activation of NLRP1 inflammasome. RESULTS: Here, AD mice have serious cognitive impairment. Meantime, Aβ was highly expressed in the brains of AD mice. SCH could effectively rescue the cognitive impairment in AD mice and impede the production of Aβ. Subsequently, we further demonstrated that SCH repressed neuronal apoptosis, pyroptosis-related proteins expression, and the activation of NLRP1 inflammasome in the hippocampus of AD mice. We also proved that Aβ induced neuronal apoptosis and pyroptosis in vitro. However, the effects of Aβ on neuronal apoptosis and pyroptosis were partly reversed by SCH treatment. CONCLUSION: Overall, our data indicated that SCH improved cognitive impairment in AD mice through inhibition of NLRP1 inflammasome-mediated neuronal pyroptosis and neuronal apoptosis. Our works provided new evidence to support SCH acting as a potential treatment method in AD. |
format | Online Article Text |
id | pubmed-7853410 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-78534102021-02-03 Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer’s Disease Li, Quan Wang, Qi Guan, Huibo Zhou, Yanyan Liu, Li Neuropsychiatr Dis Treat Original Research BACKGROUND: In recent years, schisandrin (SCH) was proved to improve Alzheimer's Disease (AD). The aim of our study is to explore the effect of SCH on neuronal pyroptosis in the disease. METHODS: A Morris water maze test was performed to evaluate the spatial learning and memory retention of AD mouse. ELISA was fulfilled to examine the concentration of Aβ, IL-1β, and IL-18. Western blot was performed to detect the expression of apoptosis- and pyroptosis-related proteins. Besides, the neuronal apoptosis rate was examined using TUNEL assay. Immunohistochemistry was utilized to detect the activation of NLRP1 inflammasome. RESULTS: Here, AD mice have serious cognitive impairment. Meantime, Aβ was highly expressed in the brains of AD mice. SCH could effectively rescue the cognitive impairment in AD mice and impede the production of Aβ. Subsequently, we further demonstrated that SCH repressed neuronal apoptosis, pyroptosis-related proteins expression, and the activation of NLRP1 inflammasome in the hippocampus of AD mice. We also proved that Aβ induced neuronal apoptosis and pyroptosis in vitro. However, the effects of Aβ on neuronal apoptosis and pyroptosis were partly reversed by SCH treatment. CONCLUSION: Overall, our data indicated that SCH improved cognitive impairment in AD mice through inhibition of NLRP1 inflammasome-mediated neuronal pyroptosis and neuronal apoptosis. Our works provided new evidence to support SCH acting as a potential treatment method in AD. Dove 2021-01-29 /pmc/articles/PMC7853410/ /pubmed/33542629 http://dx.doi.org/10.2147/NDT.S279147 Text en © 2021 Li et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Li, Quan Wang, Qi Guan, Huibo Zhou, Yanyan Liu, Li Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer’s Disease |
title | Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer’s Disease |
title_full | Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer’s Disease |
title_fullStr | Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer’s Disease |
title_full_unstemmed | Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer’s Disease |
title_short | Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer’s Disease |
title_sort | schisandrin inhibits nlrp1 inflammasome-mediated neuronal pyroptosis in mouse models of alzheimer’s disease |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7853410/ https://www.ncbi.nlm.nih.gov/pubmed/33542629 http://dx.doi.org/10.2147/NDT.S279147 |
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