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The Traditional Chinese Medicine Gedan Jiangya Decoction Alleviates Left Ventricular Hypertrophy via Suppressing the Ras/ERK1/2 Signaling Pathway
Gedan Jiangya Decoction (GJD), a Chinese herbal medicine composed of six botanical medicines, was designed to treat hypertension (patent published number (CN114246896A)). The overexpression of the ERK (extracellular signal-regulated kinase) signaling pathway is essential in developing left ventricul...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699742/ https://www.ncbi.nlm.nih.gov/pubmed/36437833 http://dx.doi.org/10.1155/2022/6924197 |
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author | Mohammed, Shadi A. D. Liu, Hanxing Baldi, Salem Chen, Pingping Wang, Yu Lu, Fang Liu, Shumin |
author_facet | Mohammed, Shadi A. D. Liu, Hanxing Baldi, Salem Chen, Pingping Wang, Yu Lu, Fang Liu, Shumin |
author_sort | Mohammed, Shadi A. D. |
collection | PubMed |
description | Gedan Jiangya Decoction (GJD), a Chinese herbal medicine composed of six botanical medicines, was designed to treat hypertension (patent published number (CN114246896A)). The overexpression of the ERK (extracellular signal-regulated kinase) signaling pathway is essential in developing left ventricular hypertrophy (LVH). This study aimed to evaluate GJD's effects on LVH in spontaneously hypertensive rats (SHRs) and examine its potential mechanisms on Ras/ERK1/2 pathway regulation. Thirty-five ten-week-old SHRs were randomly assigned to one of five groups: GJD low dosage, medium dose, high dose, model, and captopril. Wistar–Kyoto (WKY) rats served as the control group. All rats received a 6-week treatment. The following parameters were measured: systolic (SBP) and diastolic blood pressure (DBP), left ventricular mass index (LVMI), and serum TGF-beta1. The pathologic structure was determined by H & E staining and Masson. TGF-beta1, Ras, ERK1/2, and C-Fos levels were determined using western blotting and real-time qPCR. SBP, DBP, and LVMI were reduced significantly in the GJD group compared with the model group. GJD inhibited TGF-beta1, Ras, ERK1/2, and C-Fos expression in LVH. In conclusion, GJD reduced the Ras/ERK1/2 pathway expression, which decreased hypertension-induced heart hypertrophy. GJD may protect hypertension-induced myocardial hypertrophy by altering gene expression patterns in the heart. |
format | Online Article Text |
id | pubmed-9699742 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-96997422022-11-26 The Traditional Chinese Medicine Gedan Jiangya Decoction Alleviates Left Ventricular Hypertrophy via Suppressing the Ras/ERK1/2 Signaling Pathway Mohammed, Shadi A. D. Liu, Hanxing Baldi, Salem Chen, Pingping Wang, Yu Lu, Fang Liu, Shumin Evid Based Complement Alternat Med Research Article Gedan Jiangya Decoction (GJD), a Chinese herbal medicine composed of six botanical medicines, was designed to treat hypertension (patent published number (CN114246896A)). The overexpression of the ERK (extracellular signal-regulated kinase) signaling pathway is essential in developing left ventricular hypertrophy (LVH). This study aimed to evaluate GJD's effects on LVH in spontaneously hypertensive rats (SHRs) and examine its potential mechanisms on Ras/ERK1/2 pathway regulation. Thirty-five ten-week-old SHRs were randomly assigned to one of five groups: GJD low dosage, medium dose, high dose, model, and captopril. Wistar–Kyoto (WKY) rats served as the control group. All rats received a 6-week treatment. The following parameters were measured: systolic (SBP) and diastolic blood pressure (DBP), left ventricular mass index (LVMI), and serum TGF-beta1. The pathologic structure was determined by H & E staining and Masson. TGF-beta1, Ras, ERK1/2, and C-Fos levels were determined using western blotting and real-time qPCR. SBP, DBP, and LVMI were reduced significantly in the GJD group compared with the model group. GJD inhibited TGF-beta1, Ras, ERK1/2, and C-Fos expression in LVH. In conclusion, GJD reduced the Ras/ERK1/2 pathway expression, which decreased hypertension-induced heart hypertrophy. GJD may protect hypertension-induced myocardial hypertrophy by altering gene expression patterns in the heart. Hindawi 2022-11-18 /pmc/articles/PMC9699742/ /pubmed/36437833 http://dx.doi.org/10.1155/2022/6924197 Text en Copyright © 2022 Shadi A. D. Mohammed et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Mohammed, Shadi A. D. Liu, Hanxing Baldi, Salem Chen, Pingping Wang, Yu Lu, Fang Liu, Shumin The Traditional Chinese Medicine Gedan Jiangya Decoction Alleviates Left Ventricular Hypertrophy via Suppressing the Ras/ERK1/2 Signaling Pathway |
title | The Traditional Chinese Medicine Gedan Jiangya Decoction Alleviates Left Ventricular Hypertrophy via Suppressing the Ras/ERK1/2 Signaling Pathway |
title_full | The Traditional Chinese Medicine Gedan Jiangya Decoction Alleviates Left Ventricular Hypertrophy via Suppressing the Ras/ERK1/2 Signaling Pathway |
title_fullStr | The Traditional Chinese Medicine Gedan Jiangya Decoction Alleviates Left Ventricular Hypertrophy via Suppressing the Ras/ERK1/2 Signaling Pathway |
title_full_unstemmed | The Traditional Chinese Medicine Gedan Jiangya Decoction Alleviates Left Ventricular Hypertrophy via Suppressing the Ras/ERK1/2 Signaling Pathway |
title_short | The Traditional Chinese Medicine Gedan Jiangya Decoction Alleviates Left Ventricular Hypertrophy via Suppressing the Ras/ERK1/2 Signaling Pathway |
title_sort | traditional chinese medicine gedan jiangya decoction alleviates left ventricular hypertrophy via suppressing the ras/erk1/2 signaling pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699742/ https://www.ncbi.nlm.nih.gov/pubmed/36437833 http://dx.doi.org/10.1155/2022/6924197 |
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