S-allylcysteine therapy reduces adverse cardiac remodelling after myocardial infarction in a rat model
Autor: | Shafreena Shaukat Ali, Siti Fatimah Azaharah Mohamed, Wei Boon Yap, Jalifah Latip, Anand Ramalingam, Satirah Zainalabidin |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Cardiac fibrosis Medicine (miscellaneous) Protein oxidation Sudden death Muscle hypertrophy 03 medical and health sciences 0404 agricultural biotechnology Internal medicine medicine TX341-641 Myocardial infarction 030109 nutrition & dietetics Nutrition and Dietetics biology business.industry Nutrition. Foods and food supply Angiotensin-converting enzyme 04 agricultural and veterinary sciences Hypertrophy medicine.disease 040401 food science Angiotensin II Glutathione S-allylcysteine Oxidative stress Heart failure Cardiology biology.protein business Food Science |
Zdroj: | Journal of Functional Foods, Vol 66, Iss, Pp 103750-(2020) |
ISSN: | 1756-4646 |
Popis: | 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. |
Databáze: | OpenAIRE |
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