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Electroacupuncture attenuates learning and memory impairment via activation of α7nAChR-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats

Studies have reported that electroacupuncture (EA) may reduce learning and memory impairment following cerebral ischemic injury. However, the precise mechanism of action remains unclear. In the present study, the attenuation of focal cerebral ischemia/reperfusion injury by EA in rats was investigate...

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Autores principales: Liu, Jiao, Li, Chunyan, Peng, Hongwei, Yu, Kunqiang, Tao, Jing, Lin, Ruhui, Chen, Lidian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526149/
https://www.ncbi.nlm.nih.gov/pubmed/28810545
http://dx.doi.org/10.3892/etm.2017.4622
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author Liu, Jiao
Li, Chunyan
Peng, Hongwei
Yu, Kunqiang
Tao, Jing
Lin, Ruhui
Chen, Lidian
author_facet Liu, Jiao
Li, Chunyan
Peng, Hongwei
Yu, Kunqiang
Tao, Jing
Lin, Ruhui
Chen, Lidian
author_sort Liu, Jiao
collection PubMed
description Studies have reported that electroacupuncture (EA) may reduce learning and memory impairment following cerebral ischemic injury. However, the precise mechanism of action remains unclear. In the present study, the attenuation of focal cerebral ischemia/reperfusion injury by EA in rats was investigated. EA at the Baihui (DU 20) and Shenting (DU 24) acupoints was demonstrated to significantly improve performance in the Morris water maze task, with shortened latency time and increased frequency of passing the platform. Molecular analysis revealed that EA activated the expression of α7 nicotinic acetylcholine receptors (α7nAChR) in the hippocampus. In addition, EA led to a decreased expression of the microglia/macrophage marker Iba1 and the astrocyte marker glial fibrillary acidic protein in the hippocampus. EA treatment also led to decreased production of the inflammatory cytokines tumor necrosis factor-α and interleukin-1β. Treatment with methyllycaconitine, an α7nAChR antagonist, attenuated the improvement of learning and memory following EA treatment and the inhibitory effects of EA on glial cell activation and inflammatory cytokine production. In conclusion, the findings of the present study demonstrate that EA is able to improve learning and memory function following cerebral ischemic injury via activation of α7nAChR, which significantly decreases the neuroinflammatory response.
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spelling pubmed-55261492017-08-11 Electroacupuncture attenuates learning and memory impairment via activation of α7nAChR-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats Liu, Jiao Li, Chunyan Peng, Hongwei Yu, Kunqiang Tao, Jing Lin, Ruhui Chen, Lidian Exp Ther Med Articles Studies have reported that electroacupuncture (EA) may reduce learning and memory impairment following cerebral ischemic injury. However, the precise mechanism of action remains unclear. In the present study, the attenuation of focal cerebral ischemia/reperfusion injury by EA in rats was investigated. EA at the Baihui (DU 20) and Shenting (DU 24) acupoints was demonstrated to significantly improve performance in the Morris water maze task, with shortened latency time and increased frequency of passing the platform. Molecular analysis revealed that EA activated the expression of α7 nicotinic acetylcholine receptors (α7nAChR) in the hippocampus. In addition, EA led to a decreased expression of the microglia/macrophage marker Iba1 and the astrocyte marker glial fibrillary acidic protein in the hippocampus. EA treatment also led to decreased production of the inflammatory cytokines tumor necrosis factor-α and interleukin-1β. Treatment with methyllycaconitine, an α7nAChR antagonist, attenuated the improvement of learning and memory following EA treatment and the inhibitory effects of EA on glial cell activation and inflammatory cytokine production. In conclusion, the findings of the present study demonstrate that EA is able to improve learning and memory function following cerebral ischemic injury via activation of α7nAChR, which significantly decreases the neuroinflammatory response. D.A. Spandidos 2017-08 2017-06-16 /pmc/articles/PMC5526149/ /pubmed/28810545 http://dx.doi.org/10.3892/etm.2017.4622 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Liu, Jiao
Li, Chunyan
Peng, Hongwei
Yu, Kunqiang
Tao, Jing
Lin, Ruhui
Chen, Lidian
Electroacupuncture attenuates learning and memory impairment via activation of α7nAChR-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats
title Electroacupuncture attenuates learning and memory impairment via activation of α7nAChR-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats
title_full Electroacupuncture attenuates learning and memory impairment via activation of α7nAChR-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats
title_fullStr Electroacupuncture attenuates learning and memory impairment via activation of α7nAChR-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats
title_full_unstemmed Electroacupuncture attenuates learning and memory impairment via activation of α7nAChR-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats
title_short Electroacupuncture attenuates learning and memory impairment via activation of α7nAChR-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats
title_sort electroacupuncture attenuates learning and memory impairment via activation of α7nachr-mediated anti-inflammatory activity in focal cerebral ischemia/reperfusion injured rats
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526149/
https://www.ncbi.nlm.nih.gov/pubmed/28810545
http://dx.doi.org/10.3892/etm.2017.4622
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