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Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway
Cerebral ischemia/reperfusion (CIR) injury occurs when blood flow is restored in the brain, causing secondary damage to the ischemic tissues. Previous studies have shown that electroacupuncture (EA) treatment contributes to brain protection against CIR injury through modulating autophagy. Studies in...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7377856/ https://www.ncbi.nlm.nih.gov/pubmed/32620714 http://dx.doi.org/10.18632/aging.103420 |
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author | Mei, Zhi-Gang Huang, Ya-Guang Feng, Zhi-Tao Luo, Ya-Nan Yang, Song-Bai Du, Li-Peng Jiang, Kang Liu, Xiao-Lu Fu, Xian-Yun Deng, Yi-Hui Zhou, Hua-Jun |
author_facet | Mei, Zhi-Gang Huang, Ya-Guang Feng, Zhi-Tao Luo, Ya-Nan Yang, Song-Bai Du, Li-Peng Jiang, Kang Liu, Xiao-Lu Fu, Xian-Yun Deng, Yi-Hui Zhou, Hua-Jun |
author_sort | Mei, Zhi-Gang |
collection | PubMed |
description | Cerebral ischemia/reperfusion (CIR) injury occurs when blood flow is restored in the brain, causing secondary damage to the ischemic tissues. Previous studies have shown that electroacupuncture (EA) treatment contributes to brain protection against CIR injury through modulating autophagy. Studies indicated that SIRT1-FOXO1 plays a crucial role in regulating autophagy. Here we investigated the mechanisms underlying the neuroprotective effect of EA and its role in modulating autophagy via the SIRT1-FOXO1 signaling pathway in rats with CIR injury. EA pretreatment at “Baihui”, “Quchi” and “Zusanli” acupoints (2/15Hz, 1mA, 30 min/day) was performed for 5 days before the rats were subjected to middle cerebral artery occlusion, and the results indicated that EA pretreatment substantially reduced the Longa score and infarct volume, increased the dendritic spine density and lessened autophagosomes in the peri-ischemic cortex of rats. Additionally, EA pretreatment also reduced the ratio of LC3-II/LC3-I, the levels of Ac-FOXO1 and Atg7, and the interaction of Ac-FOXO1 and Atg7, but increased the levels of p62, SIRT1, and FOXO1. The above effects were abrogated by the SIRT1 inhibitor EX527. Thus, we presume that EA pretreatment elicits a neuroprotective effect against CIR injury, potentially by suppressing autophagy via activating the SIRT1-FOXO1 signaling pathway. |
format | Online Article Text |
id | pubmed-7377856 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-73778562020-07-31 Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway Mei, Zhi-Gang Huang, Ya-Guang Feng, Zhi-Tao Luo, Ya-Nan Yang, Song-Bai Du, Li-Peng Jiang, Kang Liu, Xiao-Lu Fu, Xian-Yun Deng, Yi-Hui Zhou, Hua-Jun Aging (Albany NY) Research Paper Cerebral ischemia/reperfusion (CIR) injury occurs when blood flow is restored in the brain, causing secondary damage to the ischemic tissues. Previous studies have shown that electroacupuncture (EA) treatment contributes to brain protection against CIR injury through modulating autophagy. Studies indicated that SIRT1-FOXO1 plays a crucial role in regulating autophagy. Here we investigated the mechanisms underlying the neuroprotective effect of EA and its role in modulating autophagy via the SIRT1-FOXO1 signaling pathway in rats with CIR injury. EA pretreatment at “Baihui”, “Quchi” and “Zusanli” acupoints (2/15Hz, 1mA, 30 min/day) was performed for 5 days before the rats were subjected to middle cerebral artery occlusion, and the results indicated that EA pretreatment substantially reduced the Longa score and infarct volume, increased the dendritic spine density and lessened autophagosomes in the peri-ischemic cortex of rats. Additionally, EA pretreatment also reduced the ratio of LC3-II/LC3-I, the levels of Ac-FOXO1 and Atg7, and the interaction of Ac-FOXO1 and Atg7, but increased the levels of p62, SIRT1, and FOXO1. The above effects were abrogated by the SIRT1 inhibitor EX527. Thus, we presume that EA pretreatment elicits a neuroprotective effect against CIR injury, potentially by suppressing autophagy via activating the SIRT1-FOXO1 signaling pathway. Impact Journals 2020-07-03 /pmc/articles/PMC7377856/ /pubmed/32620714 http://dx.doi.org/10.18632/aging.103420 Text en Copyright © 2020 Mei et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Mei, Zhi-Gang Huang, Ya-Guang Feng, Zhi-Tao Luo, Ya-Nan Yang, Song-Bai Du, Li-Peng Jiang, Kang Liu, Xiao-Lu Fu, Xian-Yun Deng, Yi-Hui Zhou, Hua-Jun Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway |
title | Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway |
title_full | Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway |
title_fullStr | Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway |
title_full_unstemmed | Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway |
title_short | Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway |
title_sort | electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the sirt1-foxo1 signaling pathway |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7377856/ https://www.ncbi.nlm.nih.gov/pubmed/32620714 http://dx.doi.org/10.18632/aging.103420 |
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