S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model

Adverse cardiac remodelling such as hypertrophy and fibrosis are strong determinants of heart failure and sudden death after myocardial infarction (MI). This study investigated the impact of S-allylcysteine therapy on adverse cardiac remodelling after MI in a preclinical rat model. Wistar rats (n = ...

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Main Authors: Satirah Zainalabidin, Anand Ramalingam, Siti Fatimah Azaharah Mohamed, Shafreena Shaukat Ali, Jalifah Latip, Wei Boon Yap
Format: Article
Language:English
Published: Elsevier 2020-03-01
Series:Journal of Functional Foods
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S1756464619306747
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author Satirah Zainalabidin
Anand Ramalingam
Siti Fatimah Azaharah Mohamed
Shafreena Shaukat Ali
Jalifah Latip
Wei Boon Yap
author_facet Satirah Zainalabidin
Anand Ramalingam
Siti Fatimah Azaharah Mohamed
Shafreena Shaukat Ali
Jalifah Latip
Wei Boon Yap
author_sort Satirah Zainalabidin
collection DOAJ
description Adverse cardiac remodelling such as hypertrophy and fibrosis are strong determinants of heart failure and sudden death after myocardial infarction (MI). This study investigated the impact of S-allylcysteine therapy on adverse cardiac remodelling after MI in a preclinical rat model. Wistar rats (n = 6–8/group) were subjected to MI via isoprenaline overdose and were then administered with S-allylcysteine (50 or 100 mg/kg) orally for 7 days. Compared to the sham controls, untreated MI rats showed enhanced cardiac hypertrophy and fibrosis 7 days after MI, accompanied by a significant reduction in left ventricle glutathione and glutathione reductase activities with concomitant increase in protein oxidation. S-allylcysteine therapy however, significantly attenuated cardiac hypertrophy, fibrosis and oxidative stress after MI. S-allylcysteine therapy also prevented upregulation of angiotensin converting enzyme and angiotensin II type I receptor in these rat hearts. These findings altogether suggested that S-allylcysteine therapy reduced adverse cardiac remodelling after MI in rats.
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spelling doaj.art-1af4a22ba39f48989eb14ea7ffc464372022-12-21T23:22:21ZengElsevierJournal of Functional Foods1756-46462020-03-0166103750S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat modelSatirah Zainalabidin0Anand Ramalingam1Siti Fatimah Azaharah Mohamed2Shafreena Shaukat Ali3Jalifah Latip4Wei Boon Yap5Programme of Biomedical Science, Centre for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur 50300, Malaysia; Corresponding author at: Centre for Applied and Health Sciences, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, Malaysia.Programme of Biomedical Science, Centre for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur 50300, MalaysiaProgramme of Biomedical Science, Centre for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur 50300, MalaysiaProgramme of Biomedical Science, Centre for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur 50300, MalaysiaSchool of Chemical Sciences and Food Technology, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, 43600 Bangi, Selangor, MalaysiaProgramme of Biomedical Science, Centre for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur 50300, MalaysiaAdverse cardiac remodelling such as hypertrophy and fibrosis are strong determinants of heart failure and sudden death after myocardial infarction (MI). This study investigated the impact of S-allylcysteine therapy on adverse cardiac remodelling after MI in a preclinical rat model. Wistar rats (n = 6–8/group) were subjected to MI via isoprenaline overdose and were then administered with S-allylcysteine (50 or 100 mg/kg) orally for 7 days. Compared to the sham controls, untreated MI rats showed enhanced cardiac hypertrophy and fibrosis 7 days after MI, accompanied by a significant reduction in left ventricle glutathione and glutathione reductase activities with concomitant increase in protein oxidation. S-allylcysteine therapy however, significantly attenuated cardiac hypertrophy, fibrosis and oxidative stress after MI. S-allylcysteine therapy also prevented upregulation of angiotensin converting enzyme and angiotensin II type I receptor in these rat hearts. These findings altogether suggested that S-allylcysteine therapy reduced adverse cardiac remodelling after MI in rats.http://www.sciencedirect.com/science/article/pii/S1756464619306747Cardiac fibrosisGlutathioneHypertrophyOxidative stressS-allylcysteine
spellingShingle Satirah Zainalabidin
Anand Ramalingam
Siti Fatimah Azaharah Mohamed
Shafreena Shaukat Ali
Jalifah Latip
Wei Boon Yap
S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model
Journal of Functional Foods
Cardiac fibrosis
Glutathione
Hypertrophy
Oxidative stress
S-allylcysteine
title S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model
title_full S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model
title_fullStr S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model
title_full_unstemmed S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model
title_short S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model
title_sort s allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model
topic Cardiac fibrosis
Glutathione
Hypertrophy
Oxidative stress
S-allylcysteine
url http://www.sciencedirect.com/science/article/pii/S1756464619306747
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