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Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction
Background: Myocardial infarction (MI), a life-threatening disorder, arises from the imbalance between oxygen supply and myocardial demand. Linalool is a naturally occurring monoterpenes with proved numerous pharmacological actions. This study investigated the cardioprotective effect of Linalool on...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7915311/ https://www.ncbi.nlm.nih.gov/pubmed/33562483 http://dx.doi.org/10.3390/life11020120 |
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author | Mohamed, Maged E. Abduldaium, Mohamed S. Younis, Nancy S. |
author_facet | Mohamed, Maged E. Abduldaium, Mohamed S. Younis, Nancy S. |
author_sort | Mohamed, Maged E. |
collection | PubMed |
description | Background: Myocardial infarction (MI), a life-threatening disorder, arises from the imbalance between oxygen supply and myocardial demand. Linalool is a naturally occurring monoterpenes with proved numerous pharmacological actions. This study investigated the cardioprotective effect of Linalool on isoproterenol (ISO)-induced MI in rat models and explored part of the underlying molecular mechanisms. Methods: Rats were divided into five groups; groups I and II served as normal and linalool control groups, Group III administered ISO alone; groups V and VI received two different doses of Linalool and were challenged by ISO. Different biochemical parameters were determined, including hemodynamic, infarction size, cardiac enzymes, apoptotic markers, and inflammatory mediators. Results: Linalool limited the infarcted area size and diminished the elevated cardiac enzymes. Linalool escalated HO-1 and Nrf2, both nuclear and cytosol fractions, and reduced Keap 1. Linalool enhanced cardiac antioxidant activities, reduced inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), nuclear factor-κ-B (NF-κB), interleukin 1 beta (IL-1β), interleukin 6 (IL-6)), apoptotic markers (Caspase-3, Caspase-9, and Bax), and elevated Bcl2. Conclusion: Linalool could act as an effective cardioprotective agent in the MI model through improving the oxidative condition, probably via the Nrf2/HO-1 pathway and by abolishing both apoptotic and inflammatory responses. |
format | Online Article Text |
id | pubmed-7915311 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-79153112021-03-01 Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction Mohamed, Maged E. Abduldaium, Mohamed S. Younis, Nancy S. Life (Basel) Article Background: Myocardial infarction (MI), a life-threatening disorder, arises from the imbalance between oxygen supply and myocardial demand. Linalool is a naturally occurring monoterpenes with proved numerous pharmacological actions. This study investigated the cardioprotective effect of Linalool on isoproterenol (ISO)-induced MI in rat models and explored part of the underlying molecular mechanisms. Methods: Rats were divided into five groups; groups I and II served as normal and linalool control groups, Group III administered ISO alone; groups V and VI received two different doses of Linalool and were challenged by ISO. Different biochemical parameters were determined, including hemodynamic, infarction size, cardiac enzymes, apoptotic markers, and inflammatory mediators. Results: Linalool limited the infarcted area size and diminished the elevated cardiac enzymes. Linalool escalated HO-1 and Nrf2, both nuclear and cytosol fractions, and reduced Keap 1. Linalool enhanced cardiac antioxidant activities, reduced inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), nuclear factor-κ-B (NF-κB), interleukin 1 beta (IL-1β), interleukin 6 (IL-6)), apoptotic markers (Caspase-3, Caspase-9, and Bax), and elevated Bcl2. Conclusion: Linalool could act as an effective cardioprotective agent in the MI model through improving the oxidative condition, probably via the Nrf2/HO-1 pathway and by abolishing both apoptotic and inflammatory responses. MDPI 2021-02-05 /pmc/articles/PMC7915311/ /pubmed/33562483 http://dx.doi.org/10.3390/life11020120 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Mohamed, Maged E. Abduldaium, Mohamed S. Younis, Nancy S. Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction |
title | Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction |
title_full | Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction |
title_fullStr | Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction |
title_full_unstemmed | Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction |
title_short | Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction |
title_sort | cardioprotective effect of linalool against isoproterenol-induced myocardial infarction |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7915311/ https://www.ncbi.nlm.nih.gov/pubmed/33562483 http://dx.doi.org/10.3390/life11020120 |
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