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Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice

BACKGROUND: Postoperative cognitive dysfunction (POCD) is associated with worsened prognosis especially in aged population. Clinical and animal studies suggested that electroacupuncture (EA) could improve POCD. However, the underlying mechanisms especially EA’s regulatory role of inflammasomes remai...

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Autores principales: Sun, Long, Yong, Yue, Wei, Pan, Wang, Yongqiang, Li, He, Zhou, Yalan, Ruan, Wenqing, Li, Xing, Song, Jiangang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8841296/
https://www.ncbi.nlm.nih.gov/pubmed/34951130
http://dx.doi.org/10.1111/cns.13784
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author Sun, Long
Yong, Yue
Wei, Pan
Wang, Yongqiang
Li, He
Zhou, Yalan
Ruan, Wenqing
Li, Xing
Song, Jiangang
author_facet Sun, Long
Yong, Yue
Wei, Pan
Wang, Yongqiang
Li, He
Zhou, Yalan
Ruan, Wenqing
Li, Xing
Song, Jiangang
author_sort Sun, Long
collection PubMed
description BACKGROUND: Postoperative cognitive dysfunction (POCD) is associated with worsened prognosis especially in aged population. Clinical and animal studies suggested that electroacupuncture (EA) could improve POCD. However, the underlying mechanisms especially EA’s regulatory role of inflammasomes remain unclear. METHODS: The model of POCD was established by partial hepatectomy surgery in 18‐month mice with or without postoperative EA treatment to the Baihui acupoint (GV20) for 7 days. Cognitive functions were assessed by Morris water maze test, and proinflammatory cytokines IL‐1β and IL‐6 and microglia activity were assayed by qPCR, ELISA, or immunohistochemistry. Tight junction proteins, NLRP3 inflammasome and downstream proteins, and NF‐κB pathway proteins were evaluated by western blotting. RESULTS: EA markedly preserved cognitive dysfunctions in POCD mice, associated with the inhibition of neuroinflammation as evidenced by reduced microglial activation and decreased IL‐1β and IL‐6 levels in brain tissue. EA also preserved hippocampal neurons and tight junction proteins ZO‐1 and claudin 5. Mechanistically, the activation of NLRP3 inflammasome and NF‐κB was inhibited by EA, while NLRP3 activation abolished EA’s treatment effects on cognitive function. CONCLUSION: EA alleviates POCD‐mediated cognitive dysfunction associated with ameliorated neuroinflammation. Mechanistically, EA’s treatment effects are dependent on NLRP3 inhibition.
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spelling pubmed-88412962022-02-22 Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice Sun, Long Yong, Yue Wei, Pan Wang, Yongqiang Li, He Zhou, Yalan Ruan, Wenqing Li, Xing Song, Jiangang CNS Neurosci Ther Original Articles BACKGROUND: Postoperative cognitive dysfunction (POCD) is associated with worsened prognosis especially in aged population. Clinical and animal studies suggested that electroacupuncture (EA) could improve POCD. However, the underlying mechanisms especially EA’s regulatory role of inflammasomes remain unclear. METHODS: The model of POCD was established by partial hepatectomy surgery in 18‐month mice with or without postoperative EA treatment to the Baihui acupoint (GV20) for 7 days. Cognitive functions were assessed by Morris water maze test, and proinflammatory cytokines IL‐1β and IL‐6 and microglia activity were assayed by qPCR, ELISA, or immunohistochemistry. Tight junction proteins, NLRP3 inflammasome and downstream proteins, and NF‐κB pathway proteins were evaluated by western blotting. RESULTS: EA markedly preserved cognitive dysfunctions in POCD mice, associated with the inhibition of neuroinflammation as evidenced by reduced microglial activation and decreased IL‐1β and IL‐6 levels in brain tissue. EA also preserved hippocampal neurons and tight junction proteins ZO‐1 and claudin 5. Mechanistically, the activation of NLRP3 inflammasome and NF‐κB was inhibited by EA, while NLRP3 activation abolished EA’s treatment effects on cognitive function. CONCLUSION: EA alleviates POCD‐mediated cognitive dysfunction associated with ameliorated neuroinflammation. Mechanistically, EA’s treatment effects are dependent on NLRP3 inhibition. John Wiley and Sons Inc. 2021-12-23 /pmc/articles/PMC8841296/ /pubmed/34951130 http://dx.doi.org/10.1111/cns.13784 Text en © 2021 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Sun, Long
Yong, Yue
Wei, Pan
Wang, Yongqiang
Li, He
Zhou, Yalan
Ruan, Wenqing
Li, Xing
Song, Jiangang
Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice
title Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice
title_full Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice
title_fullStr Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice
title_full_unstemmed Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice
title_short Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice
title_sort electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via nlrp3 signal inhibition in aged mice
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8841296/
https://www.ncbi.nlm.nih.gov/pubmed/34951130
http://dx.doi.org/10.1111/cns.13784
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