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Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state
BACKGROUND: Glycyrrhizic acid (GA), a bioactive triterpenoid saponin isolated from the roots of licorice plants (Glycyrrhiza glabra), has been shown to exert a variety of pharmacological activities and is considered to have potential therapeutic applications. The purpose of the present study was to...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove Medical Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5965375/ https://www.ncbi.nlm.nih.gov/pubmed/29849452 http://dx.doi.org/10.2147/DDDT.S165225 |
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author | Xu, Chongli Liang, Caihong Sun, Weixin Chen, Jiandong Chen, Xiaohu |
author_facet | Xu, Chongli Liang, Caihong Sun, Weixin Chen, Jiandong Chen, Xiaohu |
author_sort | Xu, Chongli |
collection | PubMed |
description | BACKGROUND: Glycyrrhizic acid (GA), a bioactive triterpenoid saponin isolated from the roots of licorice plants (Glycyrrhiza glabra), has been shown to exert a variety of pharmacological activities and is considered to have potential therapeutic applications. The purpose of the present study was to investigate the cardioprotective effect of GA on myocardial ischemia (MI) injury rats induced by isoproterenol (ISO), and explore the potential mechanisms underlying these effects. MATERIALS AND METHODS: The rats were randomized into five groups: control, ISO, ISO+diltiazem (10 mg/kg), ISO+GA (10 mg/kg), and ISO+GA (20 mg/kg). Electrocardiogram and histopathological examination were performed. Markers of cardiac marker enzymes (creatine kinase-MB, lactate dehydrogenase), oxidative stress (superoxide dismutase, malondialdehyde [MDA]), and inflammation (TNF-α, IL-1β, and IL-6) were also measured in each group. Proteins involved in NF-κB and Nrf-2/HO-1 pathway were detected by Western blot. RESULTS: GA decreased the ST elevation induced by MI, decreased serum levels of creatine kinase, lactate dehydrogenase, malondialdehyde, IL-6, IL-1β, and TNF-α, and increased serum superoxide dismutase and malondialdehyde activities. Furthermore, GA increased the protein levels of Nrf-2 and HO-1 and downregulated the phosphorylation of IκB, and NF-κB p65 in ISO-induced MI. CONCLUSION: These observations indicated that GA has cardioprotective effects against MI, and these effects might be related to the activation of Nrf-2/HO-1 and inhibition of NF-κB signaling pathway in the myocardium. |
format | Online Article Text |
id | pubmed-5965375 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-59653752018-05-30 Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state Xu, Chongli Liang, Caihong Sun, Weixin Chen, Jiandong Chen, Xiaohu Drug Des Devel Ther Original Research BACKGROUND: Glycyrrhizic acid (GA), a bioactive triterpenoid saponin isolated from the roots of licorice plants (Glycyrrhiza glabra), has been shown to exert a variety of pharmacological activities and is considered to have potential therapeutic applications. The purpose of the present study was to investigate the cardioprotective effect of GA on myocardial ischemia (MI) injury rats induced by isoproterenol (ISO), and explore the potential mechanisms underlying these effects. MATERIALS AND METHODS: The rats were randomized into five groups: control, ISO, ISO+diltiazem (10 mg/kg), ISO+GA (10 mg/kg), and ISO+GA (20 mg/kg). Electrocardiogram and histopathological examination were performed. Markers of cardiac marker enzymes (creatine kinase-MB, lactate dehydrogenase), oxidative stress (superoxide dismutase, malondialdehyde [MDA]), and inflammation (TNF-α, IL-1β, and IL-6) were also measured in each group. Proteins involved in NF-κB and Nrf-2/HO-1 pathway were detected by Western blot. RESULTS: GA decreased the ST elevation induced by MI, decreased serum levels of creatine kinase, lactate dehydrogenase, malondialdehyde, IL-6, IL-1β, and TNF-α, and increased serum superoxide dismutase and malondialdehyde activities. Furthermore, GA increased the protein levels of Nrf-2 and HO-1 and downregulated the phosphorylation of IκB, and NF-κB p65 in ISO-induced MI. CONCLUSION: These observations indicated that GA has cardioprotective effects against MI, and these effects might be related to the activation of Nrf-2/HO-1 and inhibition of NF-κB signaling pathway in the myocardium. Dove Medical Press 2018-05-18 /pmc/articles/PMC5965375/ /pubmed/29849452 http://dx.doi.org/10.2147/DDDT.S165225 Text en © 2018 Xu et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Xu, Chongli Liang, Caihong Sun, Weixin Chen, Jiandong Chen, Xiaohu Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state |
title | Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state |
title_full | Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state |
title_fullStr | Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state |
title_full_unstemmed | Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state |
title_short | Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state |
title_sort | glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5965375/ https://www.ncbi.nlm.nih.gov/pubmed/29849452 http://dx.doi.org/10.2147/DDDT.S165225 |
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