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Ginsenoside Rb1 improves cardiac function and remodeling in heart failure
We investigated the effect of ginsenoside Rb1 on cardiac function and remodeling in heart failure (HF). Four weeks after HF induction, the rats were administrated with ginsenoside Rb1 (35 and 70 mg/kg) and losartan (4.5 mg/kg) for 8 weeks. Losartan was used as a positive control. Cardiac function wa...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Japanese Association for Laboratory Animal Science
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5543242/ https://www.ncbi.nlm.nih.gov/pubmed/28367863 http://dx.doi.org/10.1538/expanim.16-0121 |
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author | Zheng, Xian Wang, Shuai Zou, Xiaoming Jing, Yating Yang, Ronglai Li, Siqi Wang, Fengrong |
author_facet | Zheng, Xian Wang, Shuai Zou, Xiaoming Jing, Yating Yang, Ronglai Li, Siqi Wang, Fengrong |
author_sort | Zheng, Xian |
collection | PubMed |
description | We investigated the effect of ginsenoside Rb1 on cardiac function and remodeling in heart failure (HF). Four weeks after HF induction, the rats were administrated with ginsenoside Rb1 (35 and 70 mg/kg) and losartan (4.5 mg/kg) for 8 weeks. Losartan was used as a positive control. Cardiac function was assessed by measuring hemodynamic parameters. Histological changes were analyzed by HE and Masson’s trichrome staining. Cardiac hypertrophy, fibrosis, mitochondrial membrane potential and glucose transporter type 4 (GLUT4) levels were evaluated. In the present study, high dose of (H−) ginsenoside Rb1 decreased heart rate, improved cardiac function and alleviated histological changes induced by HF. H-ginsenoside Rb1 attenuated cardiac hypertrophy and myocardial fibrosis by decreasing left ventricular (LV) weight/heart weight ratio and cardiomyocyte cross-sectional area and reducing the levels of atrial natriuretic factor (ANF), β-myosin heavy chain (β-MHC), periostin, collagen I, Angiotensin II (Ang II), Angiotensin converting enzyme (ACE) and Ang II type 1 (AT1) receptor. Moreover, H-ginsenoside Rb1 decreased mitochondrial membrane potential and enhanced the translocation of GLUT4 to plasma membrane. The TGF-β1/Smad and ERK signaling pathways were inhibited and the Akt pathway was activated. These findings suggest that ginsenoside Rb1 might restore cardiac/mitochondrial function, increase glucose uptake and protect against cardiac remodeling via the TGF-β1/Smad, ERK and Akt signaling pathways. |
format | Online Article Text |
id | pubmed-5543242 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Japanese Association for Laboratory Animal Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-55432422017-08-09 Ginsenoside Rb1 improves cardiac function and remodeling in heart failure Zheng, Xian Wang, Shuai Zou, Xiaoming Jing, Yating Yang, Ronglai Li, Siqi Wang, Fengrong Exp Anim Original We investigated the effect of ginsenoside Rb1 on cardiac function and remodeling in heart failure (HF). Four weeks after HF induction, the rats were administrated with ginsenoside Rb1 (35 and 70 mg/kg) and losartan (4.5 mg/kg) for 8 weeks. Losartan was used as a positive control. Cardiac function was assessed by measuring hemodynamic parameters. Histological changes were analyzed by HE and Masson’s trichrome staining. Cardiac hypertrophy, fibrosis, mitochondrial membrane potential and glucose transporter type 4 (GLUT4) levels were evaluated. In the present study, high dose of (H−) ginsenoside Rb1 decreased heart rate, improved cardiac function and alleviated histological changes induced by HF. H-ginsenoside Rb1 attenuated cardiac hypertrophy and myocardial fibrosis by decreasing left ventricular (LV) weight/heart weight ratio and cardiomyocyte cross-sectional area and reducing the levels of atrial natriuretic factor (ANF), β-myosin heavy chain (β-MHC), periostin, collagen I, Angiotensin II (Ang II), Angiotensin converting enzyme (ACE) and Ang II type 1 (AT1) receptor. Moreover, H-ginsenoside Rb1 decreased mitochondrial membrane potential and enhanced the translocation of GLUT4 to plasma membrane. The TGF-β1/Smad and ERK signaling pathways were inhibited and the Akt pathway was activated. These findings suggest that ginsenoside Rb1 might restore cardiac/mitochondrial function, increase glucose uptake and protect against cardiac remodeling via the TGF-β1/Smad, ERK and Akt signaling pathways. Japanese Association for Laboratory Animal Science 2017-03-30 2017 /pmc/articles/PMC5543242/ /pubmed/28367863 http://dx.doi.org/10.1538/expanim.16-0121 Text en ©2017 Japanese Association for Laboratory Animal Science This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: https://creativecommons.org/licenses/by-nc-nd/4.0/) |
spellingShingle | Original Zheng, Xian Wang, Shuai Zou, Xiaoming Jing, Yating Yang, Ronglai Li, Siqi Wang, Fengrong Ginsenoside Rb1 improves cardiac function and remodeling in heart failure |
title | Ginsenoside Rb1 improves cardiac function and remodeling in heart
failure |
title_full | Ginsenoside Rb1 improves cardiac function and remodeling in heart
failure |
title_fullStr | Ginsenoside Rb1 improves cardiac function and remodeling in heart
failure |
title_full_unstemmed | Ginsenoside Rb1 improves cardiac function and remodeling in heart
failure |
title_short | Ginsenoside Rb1 improves cardiac function and remodeling in heart
failure |
title_sort | ginsenoside rb1 improves cardiac function and remodeling in heart
failure |
topic | Original |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5543242/ https://www.ncbi.nlm.nih.gov/pubmed/28367863 http://dx.doi.org/10.1538/expanim.16-0121 |
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