Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway

We aimed to explore the effects of emodin on the energy metabolism of myocardial cells in rats with post-myocardial infarction (MI) heart failure (HF) and the extracellular signal-regulated kinase (ERK) pathway. The model of MI was established by ligation of the left anterior descending branch. Afte...

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Autores principales:	Jinfeng Liu, Liang Ning
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	emodin myocardial infarction heart failure energy metabolism extracellular signal-regulated kinase Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/cf22cc41b22b44df93dff60e6c0a0a08
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spelling	oai:doaj.org-article:cf22cc41b22b44df93dff60e6c0a0a082021-12-01T14:41:00ZProtective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway2165-59792165-598710.1080/21655979.2021.1983977https://doaj.org/article/cf22cc41b22b44df93dff60e6c0a0a082021-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1983977https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987We aimed to explore the effects of emodin on the energy metabolism of myocardial cells in rats with post-myocardial infarction (MI) heart failure (HF) and the extracellular signal-regulated kinase (ERK) pathway. The model of MI was established by ligation of the left anterior descending branch. After 4 weeks, the rats with left ventricular ejection fraction (LVEF) of ≤45% were used aspost-MI HF model animals and randomly divided into model, low-dose, middle-dose, high-dose and control groups (n=10). Low-, middle- and high-dose groups were gavaged with 20 mg/kg, 40 mg/kg and 60 mg/kg emodin daily, respectively. After administration for 14 d, the changes in LVEF, left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD) and interventricular septum thickness (IVS) were analyzed. The apoptosis rate of myocardial cells was detected by TUNEL staining. The levels of serum cardiac troponin I (cTnI) and peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1) were determined using ELISA, and the expressions of mitochondrial respiratory chain complex I protein and phosphorylated-ERK (p-ERK) in myocardial tissues were determined by Western blotting. Compared with model group, LVEDD, LVESD, apoptosis rate of myocardial cells, levels of serum cTnI and PGC-1, and expressions of complex I and p-ERK in myocardial tissues significantly decreased, while LVEF and IVS increased in low-dose, middle-dose, high-dose and control groups (P<0.05). The changes in the above indices were significantly dependent on the dose of emodin (P<0.05).Emodin can significantly relieve post-MI HF, reduce the apoptosis rate of myocardial tissues, and ameliorate the cardiac function of rats.Jinfeng LiuLiang NingTaylor & Francis Grouparticleemodinmyocardial infarctionheart failureenergy metabolismextracellular signal-regulated kinaseBiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 2, Pp 10246-10253 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	emodin myocardial infarction heart failure energy metabolism extracellular signal-regulated kinase Biotechnology TP248.13-248.65
spellingShingle	emodin myocardial infarction heart failure energy metabolism extracellular signal-regulated kinase Biotechnology TP248.13-248.65 Jinfeng Liu Liang Ning Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway
description	We aimed to explore the effects of emodin on the energy metabolism of myocardial cells in rats with post-myocardial infarction (MI) heart failure (HF) and the extracellular signal-regulated kinase (ERK) pathway. The model of MI was established by ligation of the left anterior descending branch. After 4 weeks, the rats with left ventricular ejection fraction (LVEF) of ≤45% were used aspost-MI HF model animals and randomly divided into model, low-dose, middle-dose, high-dose and control groups (n=10). Low-, middle- and high-dose groups were gavaged with 20 mg/kg, 40 mg/kg and 60 mg/kg emodin daily, respectively. After administration for 14 d, the changes in LVEF, left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD) and interventricular septum thickness (IVS) were analyzed. The apoptosis rate of myocardial cells was detected by TUNEL staining. The levels of serum cardiac troponin I (cTnI) and peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1) were determined using ELISA, and the expressions of mitochondrial respiratory chain complex I protein and phosphorylated-ERK (p-ERK) in myocardial tissues were determined by Western blotting. Compared with model group, LVEDD, LVESD, apoptosis rate of myocardial cells, levels of serum cTnI and PGC-1, and expressions of complex I and p-ERK in myocardial tissues significantly decreased, while LVEF and IVS increased in low-dose, middle-dose, high-dose and control groups (P<0.05). The changes in the above indices were significantly dependent on the dose of emodin (P<0.05).Emodin can significantly relieve post-MI HF, reduce the apoptosis rate of myocardial tissues, and ameliorate the cardiac function of rats.
format	article
author	Jinfeng Liu Liang Ning
author_facet	Jinfeng Liu Liang Ning
author_sort	Jinfeng Liu
title	Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway
title_short	Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway
title_full	Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway
title_fullStr	Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway
title_full_unstemmed	Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway
title_sort	protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/cf22cc41b22b44df93dff60e6c0a0a08
work_keys_str_mv	AT jinfengliu protectiveroleofemodininratswithpostmyocardialinfarctionheartfailureandinfluenceonextracellularsignalregulatedkinasepathway AT liangning protectiveroleofemodininratswithpostmyocardialinfarctionheartfailureandinfluenceonextracellularsignalregulatedkinasepathway
_version_	1718405022813782016

Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway

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