This study presents a novel mechanistic insight into the anti-acute myocardial infarction effects of allicin and highlights the therapeutic potential of this compound. - GreenMedInfo Summary

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 (HS) synthetase inhibitor, was used to examine the effects of allicin on HS production. Isolated coronary arteries and cardiomyocytes were assessed for vascular reactivity and cellular Catransport 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 HS and HS synthetase levels. Allicin administration resulted in concentration-dependent effects on coronary artery dilation, which were mediated by receptor-dependent Cachannels, ATP-sensitive Kchannels, and sarcoplasmic reticulum (SR) Carelease induced by the ryanodine receptor. Allicin administration improved Cahomeostasis in cardiomyocytes by increasing cardiomyocyte contraction, Catransient amplitude, myofilament sensitivity, and SR Cacontent. Allicin also enhanced Cauptake via SR Ca-ATPase and Caremoval via the Na/Caexchanger, and it reduced SR Caleakage. Notably, the protective effects of allicin were partially attenuated by blockade of HS production with PAG. Our findings provide novel evidence that allicin-induced production of HS mediates coronary artery dilation and regulation of Cahomeostasis in AMI. Our study presents a novel mechanistic insight into the anti-AMI effects of allicin and highlights the therapeutic potential of this compound.