HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/5/H2693    most recent 00853.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Chuah, S. C. Articles by Zhu, Y. Z. Search for Related Content PubMed PubMed Citation Articles by Chuah, S. C. Articles by Zhu, Y. Z.

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

¹Cardiovascular Biology Research Group, Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; and ²Department of Pharmacology, School of Pharmacy and Institute of Biomedical Sciences, Fudan University, Shanghai, China

Submitted 22 July 2007 ; accepted in final form 30 August 2007

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·kg^–1·day^–1), SAC + propagylglycine (PAG; 50 mg + 10 mg·kg^–1·day^–1) or PAG (10 mg·kg^–1·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--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 µmol·g protein^–1·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 µmol·g protein^–1·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.

S-allylcysteine; garlic; hydrogen sulfide; myocardial infarction; cardioprotection