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Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca(2+) influx via L‐type Ca(2+) channels

18β‐Glycyrrhetinic acid (18β‐GA) is a component extracted from licorice. This study aimed to evaluate the effects of 18β‐GA on isoproterenol (ISO)‐induced acute myocardial infarction in rats and mice. Two consecutive days of subcutaneous injection of ISO (85 mg/kg/day) resulted in acute myocardial i...

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Autores principales: Chu, Sijie, Wang, Weijie, Zhang, Ning, Liu, Tong, Li, Jing, Chu, Xi, Zuo, Saijie, Ma, Zhihong, Ma, Donglai, Chu, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8645779/
https://www.ncbi.nlm.nih.gov/pubmed/34925811
http://dx.doi.org/10.1002/fsn3.2639
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author Chu, Sijie
Wang, Weijie
Zhang, Ning
Liu, Tong
Li, Jing
Chu, Xi
Zuo, Saijie
Ma, Zhihong
Ma, Donglai
Chu, Li
author_facet Chu, Sijie
Wang, Weijie
Zhang, Ning
Liu, Tong
Li, Jing
Chu, Xi
Zuo, Saijie
Ma, Zhihong
Ma, Donglai
Chu, Li
author_sort Chu, Sijie
collection PubMed
description 18β‐Glycyrrhetinic acid (18β‐GA) is a component extracted from licorice. This study aimed to evaluate the effects of 18β‐GA on isoproterenol (ISO)‐induced acute myocardial infarction in rats and mice. Two consecutive days of subcutaneous injection of ISO (85 mg/kg/day) resulted in acute myocardial infarction. We examined the pathological changes, oxidative stress, inflammatory response, and expression of apoptosis in mouse hearts. The expressions of phosphoinositol‐3‐kinase (PI3K), protein kinase B (Akt), and the phosphorylation levels of PI3K (p‐PI3K) and Akt (p‐Akt) were determined by western blotting. The whole‐cell patch‐clamp technique was applied to observe the L‐type Ca(2+) currents, and the Ion Optix detection system was used for cell contraction and Ca(2+) transient in isolated rat cardiac ventricular myocytes. In ISO‐induced myocardial infarction, the J‐point, heart rate, creatine kinase, lactate dehydrogenase, superoxide dismutase, catalase, malondialdehyde, glutathion, and reactive oxygen species decreased in mice after 18β‐GA treatment. 18β‐GA improved ISO‐induced morphologic pathology, inhibited the inflammatory pathway response and cardiomyocyte apoptosis, and inhibited PI3K/Akt signaling. 18β‐GA could significantly inhibit I(Ca‐L), myocardial contraction, and Ca(2+) transient. This study demonstrates that 18β‐GA has cardioprotective effects on acute myocardial infarction, which may be related to inhibiting oxidative stress, inflammation, apoptosis via the PI3K/Akt pathway, and reducing cell contractility and Ca(2+) concentration via L‐type Ca(2+) channels.
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spelling pubmed-86457792021-12-17 Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca(2+) influx via L‐type Ca(2+) channels Chu, Sijie Wang, Weijie Zhang, Ning Liu, Tong Li, Jing Chu, Xi Zuo, Saijie Ma, Zhihong Ma, Donglai Chu, Li Food Sci Nutr Original Research 18β‐Glycyrrhetinic acid (18β‐GA) is a component extracted from licorice. This study aimed to evaluate the effects of 18β‐GA on isoproterenol (ISO)‐induced acute myocardial infarction in rats and mice. Two consecutive days of subcutaneous injection of ISO (85 mg/kg/day) resulted in acute myocardial infarction. We examined the pathological changes, oxidative stress, inflammatory response, and expression of apoptosis in mouse hearts. The expressions of phosphoinositol‐3‐kinase (PI3K), protein kinase B (Akt), and the phosphorylation levels of PI3K (p‐PI3K) and Akt (p‐Akt) were determined by western blotting. The whole‐cell patch‐clamp technique was applied to observe the L‐type Ca(2+) currents, and the Ion Optix detection system was used for cell contraction and Ca(2+) transient in isolated rat cardiac ventricular myocytes. In ISO‐induced myocardial infarction, the J‐point, heart rate, creatine kinase, lactate dehydrogenase, superoxide dismutase, catalase, malondialdehyde, glutathion, and reactive oxygen species decreased in mice after 18β‐GA treatment. 18β‐GA improved ISO‐induced morphologic pathology, inhibited the inflammatory pathway response and cardiomyocyte apoptosis, and inhibited PI3K/Akt signaling. 18β‐GA could significantly inhibit I(Ca‐L), myocardial contraction, and Ca(2+) transient. This study demonstrates that 18β‐GA has cardioprotective effects on acute myocardial infarction, which may be related to inhibiting oxidative stress, inflammation, apoptosis via the PI3K/Akt pathway, and reducing cell contractility and Ca(2+) concentration via L‐type Ca(2+) channels. John Wiley and Sons Inc. 2021-10-24 /pmc/articles/PMC8645779/ /pubmed/34925811 http://dx.doi.org/10.1002/fsn3.2639 Text en © 2021 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Chu, Sijie
Wang, Weijie
Zhang, Ning
Liu, Tong
Li, Jing
Chu, Xi
Zuo, Saijie
Ma, Zhihong
Ma, Donglai
Chu, Li
Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca(2+) influx via L‐type Ca(2+) channels
title Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca(2+) influx via L‐type Ca(2+) channels
title_full Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca(2+) influx via L‐type Ca(2+) channels
title_fullStr Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca(2+) influx via L‐type Ca(2+) channels
title_full_unstemmed Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca(2+) influx via L‐type Ca(2+) channels
title_short Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca(2+) influx via L‐type Ca(2+) channels
title_sort protective effects of 18β‐glycyrrhetinic acid against myocardial infarction: involvement of pi3k/akt pathway activation and inhibiting ca(2+) influx via l‐type ca(2+) channels
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8645779/
https://www.ncbi.nlm.nih.gov/pubmed/34925811
http://dx.doi.org/10.1002/fsn3.2639
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