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The protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor
Hederagenin (HE) plays a protective role by inhibiting cell proliferation and ameliorating fibrosis. The current therapy for Chronic kidney disease (CKD) often result in the risks of side effects. The present study aimed to explore whether it can protect against renal fibrosis and unveil the underly...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9161953/ https://www.ncbi.nlm.nih.gov/pubmed/35322725 http://dx.doi.org/10.1080/21655979.2022.2054596 |
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author | Yang, Wei He, Lijuan |
author_facet | Yang, Wei He, Lijuan |
author_sort | Yang, Wei |
collection | PubMed |
description | Hederagenin (HE) plays a protective role by inhibiting cell proliferation and ameliorating fibrosis. The current therapy for Chronic kidney disease (CKD) often result in the risks of side effects. The present study aimed to explore whether it can protect against renal fibrosis and unveil the underlying mechanism. Transforming growth factor (TGF)-β was used to induce the fibroblasts NRK-49 F for the simulation of renal fibrosis. The cell viability and expression of fibrosis-related proteins in TGF-β-treated NRK-49 F cells was, respectively, measured by Cell Counting Kit-8 (CCK-8) and western blot. After predicting the target genes of HE, M3 receptor was measured in NRK-49 F cells treated with TGF-β alone or in combination with HE. Then, M3 receptor was silenced in TGF-β-treated NRK-49 F cells for the detection of its role in proliferation and fibrosis. Muscarinic acetylcholine receptor M3 (M3 receptor) agonist pilocarpine was further added to determine the role of M3 receptor involved. HE inhibited the proliferation and fibrosis of TGF-β-treated NRK-49 F cells. M3 receptor was predicted to be a target of HE. Moreover, interference of M3 receptor improved the proliferation and fibrosis of TGF-β-treated NRK-49 F cells. Further addition of pilocarpine reversed the inhibitory effect of HE on proliferation and fibrosis of TGF-β-treated NRK-49 F cells. HE protects against renal fibrosis in NRK-49 F cells by targeting Muscarinic acetylcholine receptor, which will provide theoretical basis for the clinical use of HE for kidney-related disease treatment. |
format | Online Article Text |
id | pubmed-9161953 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-91619532022-06-03 The protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor Yang, Wei He, Lijuan Bioengineered Review Hederagenin (HE) plays a protective role by inhibiting cell proliferation and ameliorating fibrosis. The current therapy for Chronic kidney disease (CKD) often result in the risks of side effects. The present study aimed to explore whether it can protect against renal fibrosis and unveil the underlying mechanism. Transforming growth factor (TGF)-β was used to induce the fibroblasts NRK-49 F for the simulation of renal fibrosis. The cell viability and expression of fibrosis-related proteins in TGF-β-treated NRK-49 F cells was, respectively, measured by Cell Counting Kit-8 (CCK-8) and western blot. After predicting the target genes of HE, M3 receptor was measured in NRK-49 F cells treated with TGF-β alone or in combination with HE. Then, M3 receptor was silenced in TGF-β-treated NRK-49 F cells for the detection of its role in proliferation and fibrosis. Muscarinic acetylcholine receptor M3 (M3 receptor) agonist pilocarpine was further added to determine the role of M3 receptor involved. HE inhibited the proliferation and fibrosis of TGF-β-treated NRK-49 F cells. M3 receptor was predicted to be a target of HE. Moreover, interference of M3 receptor improved the proliferation and fibrosis of TGF-β-treated NRK-49 F cells. Further addition of pilocarpine reversed the inhibitory effect of HE on proliferation and fibrosis of TGF-β-treated NRK-49 F cells. HE protects against renal fibrosis in NRK-49 F cells by targeting Muscarinic acetylcholine receptor, which will provide theoretical basis for the clinical use of HE for kidney-related disease treatment. Taylor & Francis 2022-03-24 /pmc/articles/PMC9161953/ /pubmed/35322725 http://dx.doi.org/10.1080/21655979.2022.2054596 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Yang, Wei He, Lijuan The protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor |
title | The protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor |
title_full | The protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor |
title_fullStr | The protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor |
title_full_unstemmed | The protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor |
title_short | The protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor |
title_sort | protective effect of hederagenin on renal fibrosis by targeting muscarinic acetylcholine receptor |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9161953/ https://www.ncbi.nlm.nih.gov/pubmed/35322725 http://dx.doi.org/10.1080/21655979.2022.2054596 |
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