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

[Display omitted] •S-allylcysteine therapy post MI attenuates cardiac hypertrophy in rats.•S-allylcysteine therapy post MI limits cardiac fibrosis in rats.•S-allylcysteine therapy post MI blunted oxidative stress in rats.•S-allylcysteine therapy post MI regulates ACE-AT1 axis in rats. 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.