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Exploring the mechanism of YangXue QingNao Wan based on network pharmacology in the treatment of Alzheimer’s disease
It is clinical reported that YangXue QingNao Wan (YXQNW) combined with donepezil can significantly improve the cognitive function of AD patients. However, the mechanism is not clear. A network pharmacology approach was employed to predict the protein targets and affected pathways of YXQNW in the tre...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9465410/ https://www.ncbi.nlm.nih.gov/pubmed/36105078 http://dx.doi.org/10.3389/fgene.2022.942203 |
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author | Zhang, Yuying Guo, Kaimin Zhang, Pengfei Zhang, Mengying Li, Xiaoqiang Zhou, Shuiping Sun, He Wang, Wenjia Wang, Hui Hu, Yunhui |
author_facet | Zhang, Yuying Guo, Kaimin Zhang, Pengfei Zhang, Mengying Li, Xiaoqiang Zhou, Shuiping Sun, He Wang, Wenjia Wang, Hui Hu, Yunhui |
author_sort | Zhang, Yuying |
collection | PubMed |
description | It is clinical reported that YangXue QingNao Wan (YXQNW) combined with donepezil can significantly improve the cognitive function of AD patients. However, the mechanism is not clear. A network pharmacology approach was employed to predict the protein targets and affected pathways of YXQNW in the treatment of AD. Based on random walk evaluation, the correlation between YXQNW and AD was calculated; while a variety of AD clinical approved Western drugs were compared. The targets of YXQNW were enriched and analyzed by using the TSEA platform and MetaCore. We proved that the overall correlation between YXQNW and AD is equivalent to clinical Western drugs, but the mechanism of action is very different. Firstly, YXQNW may promote cerebral blood flow velocity by regulating platelet aggregation and the vasoconstriction/relaxation signal pathway, which has been verified by clinical meta-analysis. Secondly, YXQNW may promote Aβ degradation in the liver by modulating the abnormal glucose and lipid metabolisms via the adiponectin-dependent pathway, RXR/PPAR-dependent lipid metabolism signal pathway, and fatty acid synthase activity signal pathway. We also verified whether YXQNW indeed promoted Aβ degradation in hepatic stellate cells. This work provides a novel scientific basis for the mechanism of YXQNW in the treatment of AD. |
format | Online Article Text |
id | pubmed-9465410 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-94654102022-09-13 Exploring the mechanism of YangXue QingNao Wan based on network pharmacology in the treatment of Alzheimer’s disease Zhang, Yuying Guo, Kaimin Zhang, Pengfei Zhang, Mengying Li, Xiaoqiang Zhou, Shuiping Sun, He Wang, Wenjia Wang, Hui Hu, Yunhui Front Genet Genetics It is clinical reported that YangXue QingNao Wan (YXQNW) combined with donepezil can significantly improve the cognitive function of AD patients. However, the mechanism is not clear. A network pharmacology approach was employed to predict the protein targets and affected pathways of YXQNW in the treatment of AD. Based on random walk evaluation, the correlation between YXQNW and AD was calculated; while a variety of AD clinical approved Western drugs were compared. The targets of YXQNW were enriched and analyzed by using the TSEA platform and MetaCore. We proved that the overall correlation between YXQNW and AD is equivalent to clinical Western drugs, but the mechanism of action is very different. Firstly, YXQNW may promote cerebral blood flow velocity by regulating platelet aggregation and the vasoconstriction/relaxation signal pathway, which has been verified by clinical meta-analysis. Secondly, YXQNW may promote Aβ degradation in the liver by modulating the abnormal glucose and lipid metabolisms via the adiponectin-dependent pathway, RXR/PPAR-dependent lipid metabolism signal pathway, and fatty acid synthase activity signal pathway. We also verified whether YXQNW indeed promoted Aβ degradation in hepatic stellate cells. This work provides a novel scientific basis for the mechanism of YXQNW in the treatment of AD. Frontiers Media S.A. 2022-08-29 /pmc/articles/PMC9465410/ /pubmed/36105078 http://dx.doi.org/10.3389/fgene.2022.942203 Text en Copyright © 2022 Zhang, Guo, Zhang, Zhang, Li, Zhou, Sun, Wang, Wang and Hu. https://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 | Genetics Zhang, Yuying Guo, Kaimin Zhang, Pengfei Zhang, Mengying Li, Xiaoqiang Zhou, Shuiping Sun, He Wang, Wenjia Wang, Hui Hu, Yunhui Exploring the mechanism of YangXue QingNao Wan based on network pharmacology in the treatment of Alzheimer’s disease |
title | Exploring the mechanism of YangXue QingNao Wan based on network pharmacology in the treatment of Alzheimer’s disease |
title_full | Exploring the mechanism of YangXue QingNao Wan based on network pharmacology in the treatment of Alzheimer’s disease |
title_fullStr | Exploring the mechanism of YangXue QingNao Wan based on network pharmacology in the treatment of Alzheimer’s disease |
title_full_unstemmed | Exploring the mechanism of YangXue QingNao Wan based on network pharmacology in the treatment of Alzheimer’s disease |
title_short | Exploring the mechanism of YangXue QingNao Wan based on network pharmacology in the treatment of Alzheimer’s disease |
title_sort | exploring the mechanism of yangxue qingnao wan based on network pharmacology in the treatment of alzheimer’s disease |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9465410/ https://www.ncbi.nlm.nih.gov/pubmed/36105078 http://dx.doi.org/10.3389/fgene.2022.942203 |
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