Protective Effects of Allicin on Acute Myocardial Infarction in Rats via Hydrogen Sulfide-mediated Regulation of Coronary Arterial Vasomotor Function and Myocardial Calcium Transport

Acute myocardial infarction (AMI) is a condition with high morbidity and mortality, for which effective treatments are lacking. Allicin has been reported to exert therapeutic effects on AMI, but the underlying mechanisms of its action have not been fully elucidated. To investigate this, a rat model of AMI was generated by ligating the left anterior descending branch of the coronary artery. DL-propargylglycine (PAG), a specific hydrogen sulfide (H(2)S) synthetase inhibitor, was used to examine the effects of allicin on H(2)S production. Isolated coronary arteries and cardiomyocytes were assessed for vascular reactivity and cellular Ca(2+) transport using a multiwire myography system and a cell-contraction-ion detection system, respectively. Allicin administration improved cardiac function and myocardial pathology, reduced myocardial enzyme levels, and increased H(2)S and H(2)S synthetase levels. Allicin administration resulted in concentration-dependent effects on coronary artery dilation, which were mediated by receptor-dependent Ca(2+) channels, ATP-sensitive K(+) channels, and sarcoplasmic reticulum (SR) Ca(2+) release induced by the ryanodine receptor. Allicin administration improved Ca(2+) homeostasis in cardiomyocytes by increasing cardiomyocyte contraction, Ca(2+) transient amplitude, myofilament sensitivity, and SR Ca(2+) content. Allicin also enhanced Ca(2+) uptake via SR Ca(2+)-ATPase and Ca(2+) removal via the Na(+)/Ca(2+) exchanger, and it reduced SR Ca(2+) leakage. Notably, the protective effects of allicin were partially attenuated by blockade of H(2)S production with PAG. Our findings provide novel evidence that allicin-induced production of H(2)S mediates coronary artery dilation and regulation of Ca(2+) homeostasis in AMI. Our study presents a novel mechanistic insight into the anti-AMI effects of allicin and highlights the therapeutic potential of this compound.