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Cyanidin-3-O-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF-β1/p38 MAPK/CREB signaling pathway
Pulmonary artery hypertension (PAH) is a disease with high morbidity and mortality. Cyanidin-3-O-β-glucoside (Cy-3-g), a classical anthocyanin, has a variety of biological effects. The present study evaluated whether Cy-3-g attenuated PAH, and explored the potential mechanism of action. Rats were in...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7974420/ https://www.ncbi.nlm.nih.gov/pubmed/33760143 http://dx.doi.org/10.3892/mmr.2021.11977 |
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author | Ouyang, Shao Chen, Wei Gaofeng, Zeng Changcheng, Lei Guoping, Tian Minyan, Zhu Yang, Liu Min, Yang Luo, Jiahao |
author_facet | Ouyang, Shao Chen, Wei Gaofeng, Zeng Changcheng, Lei Guoping, Tian Minyan, Zhu Yang, Liu Min, Yang Luo, Jiahao |
author_sort | Ouyang, Shao |
collection | PubMed |
description | Pulmonary artery hypertension (PAH) is a disease with high morbidity and mortality. Cyanidin-3-O-β-glucoside (Cy-3-g), a classical anthocyanin, has a variety of biological effects. The present study evaluated whether Cy-3-g attenuated PAH, and explored the potential mechanism of action. Rats were injected with monocrotaline (MCT; 60 mg per kg of body weight) and then treated with Cy-3-g (200 or 400 mg per kg of body weight) for 4 weeks. Protein expression was determined in vitro in transforming growth factor-β1 (TGF-β1)-mediated human pulmonary arterial smooth muscle cells (SMCs). The results indicated that Cy-3-g significantly inhibited the mean pulmonary artery pressure, right ventricular systolic pressure and right ventricular hypertrophy index, as well as vascular remodeling induced by MCT in PAH rats. Further experiments showed that Cy-3-g suppressed the expression of pro-inflammatory factors and enhanced the levels of anti-inflammatory factors. Cy-3-g blocked oxidative stress and improved vascular endothelial injury. Cy-3-g also reduced the proliferation of SMCs. Furthermore, the MCT- and TGF-β1-induced increase in TGF-β1, phosphorylated (p)-p38 mitogen-activated protein kinase (MAPK) and p-cAMP-response element binding protein (CREB) expression was blocked by Cy-3-g treatment in vivo and in vitro. These results indicated that Cy-3-g could prevent vascular remodeling in PAH via inhibition of the TGF-β1/p38 MAPK/CREB axis. |
format | Online Article Text |
id | pubmed-7974420 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-79744202021-03-24 Cyanidin-3-O-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF-β1/p38 MAPK/CREB signaling pathway Ouyang, Shao Chen, Wei Gaofeng, Zeng Changcheng, Lei Guoping, Tian Minyan, Zhu Yang, Liu Min, Yang Luo, Jiahao Mol Med Rep Articles Pulmonary artery hypertension (PAH) is a disease with high morbidity and mortality. Cyanidin-3-O-β-glucoside (Cy-3-g), a classical anthocyanin, has a variety of biological effects. The present study evaluated whether Cy-3-g attenuated PAH, and explored the potential mechanism of action. Rats were injected with monocrotaline (MCT; 60 mg per kg of body weight) and then treated with Cy-3-g (200 or 400 mg per kg of body weight) for 4 weeks. Protein expression was determined in vitro in transforming growth factor-β1 (TGF-β1)-mediated human pulmonary arterial smooth muscle cells (SMCs). The results indicated that Cy-3-g significantly inhibited the mean pulmonary artery pressure, right ventricular systolic pressure and right ventricular hypertrophy index, as well as vascular remodeling induced by MCT in PAH rats. Further experiments showed that Cy-3-g suppressed the expression of pro-inflammatory factors and enhanced the levels of anti-inflammatory factors. Cy-3-g blocked oxidative stress and improved vascular endothelial injury. Cy-3-g also reduced the proliferation of SMCs. Furthermore, the MCT- and TGF-β1-induced increase in TGF-β1, phosphorylated (p)-p38 mitogen-activated protein kinase (MAPK) and p-cAMP-response element binding protein (CREB) expression was blocked by Cy-3-g treatment in vivo and in vitro. These results indicated that Cy-3-g could prevent vascular remodeling in PAH via inhibition of the TGF-β1/p38 MAPK/CREB axis. D.A. Spandidos 2021-05 2021-03-09 /pmc/articles/PMC7974420/ /pubmed/33760143 http://dx.doi.org/10.3892/mmr.2021.11977 Text en Copyright: © Ouyang 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 Ouyang, Shao Chen, Wei Gaofeng, Zeng Changcheng, Lei Guoping, Tian Minyan, Zhu Yang, Liu Min, Yang Luo, Jiahao Cyanidin-3-O-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF-β1/p38 MAPK/CREB signaling pathway |
title | Cyanidin-3-O-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF-β1/p38 MAPK/CREB signaling pathway |
title_full | Cyanidin-3-O-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF-β1/p38 MAPK/CREB signaling pathway |
title_fullStr | Cyanidin-3-O-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF-β1/p38 MAPK/CREB signaling pathway |
title_full_unstemmed | Cyanidin-3-O-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF-β1/p38 MAPK/CREB signaling pathway |
title_short | Cyanidin-3-O-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF-β1/p38 MAPK/CREB signaling pathway |
title_sort | cyanidin-3-o-β-glucoside protects against pulmonary artery hypertension induced by monocrotaline via the tgf-β1/p38 mapk/creb signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7974420/ https://www.ncbi.nlm.nih.gov/pubmed/33760143 http://dx.doi.org/10.3892/mmr.2021.11977 |
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