S-allylcysteine mediates cardioprotection in an acute myocardial infarction rat model via a hydrogen sulfide-mediated pathway

S-allylcysteine (SAC) is an organosulfur-containing compound derived from garlic. Studies have shown that garlic is beneficial in the treatment of cardiovascular diseases. This study aims to elucidate if SAC is responsible for this cardioprotection using acute myocardial infarction (AMI) rat models. In addition, we hypothesized that SAC may mediate cardioprotection via a hydrogen sulfide (H2S)-related pathway. Rats were pretreated with saline, SAC (50 mg center dot kg(-1)center dot day(-1)), SAC + propagylglycine (PAG; 50 mg + 10 mg center dot kg(-1)center dot day(-1)) or PAG (10 mg center dot kg(-1)center dot day(-1)) for 7 days before AMI induction and killed 48 h after. Our results showed that SAC significantly lowered mortality (12.5% vs. 33.3%, P < 0.05) and reduced infarct size. SAC + PAG-and PAG-treated rats had larger infarct sizes than controls (60.9 +/- 0.01 and 62.0 +/- 0.03%, respectively, vs. 50.0 +/- 0.03%; P < 0.05). Pretreatment with SAC did not affect BP, but BP was significantly elevated in SAC + PAG and PAG-treated groups (P < 0.05). In addition, plasma H2S levels and left ventricular cystathionine-gamma-lyase (CSE) activities were analyzed to investigate the involvement of H2S. CSE is the enzyme responsible for H2S production in the heart. SAC increased left ventricular CSE activity in AMI rats (2.75 +/- 0.34 vs. 1.23 +/- 0.16 mu mol center dot g protein(-1)center dot h(-1); P < 0.01). SAC + PAG-treated rats had significantly lower CSE activity compared with the SAC-treated group (1.22 +/- 0.27 vs. 2.75 +/- 0.34 mu mol center dot g protein(-1)center dot h(-1); P < 0.05). Similarly, SAC-treated rats had higher plasma H2S concentration compared with controls and the SAC + PAG-treated group. Protein expression studies revealed that SAC upregulated CSE expression (1.1-fold of control; P < 0.05), whereas SAC + PAG and PAG downregulated its expression (0.88-fold of control in both groups; P < 0.005). In conclusion, our study provides novel evidence that SAC is protective in myocardial infarction via an H2S-related pathway.