Allicin is a potential hypolipidemic and antiatherogenic agent: Mechanisms of action and implicated signaling...

Allicin, an organosulfur compound derived from garlic (Allium sativum), has been extensively studied for its cardiovascular benefits. Numerous reports highlight its lipid-lowering, antioxidant, and anti-atherogenic properties. The lipid-modulating effects reported for allicin-containing preparations are evidenced by reductions in plasma cholesterol and atherosclerotic lesion development. However, because intact allicin is highly unstable and rapidly degraded under physiological conditions, these effects should be interpreted as potentially reflecting the activity of allicin-derived organosulfur metabolites as well as allicin itself. Herein, we present a comprehensive summary of the reported anti-atherogenic effects of allicin. The impact of allicin on lipid metabolism, antioxidant defenses, and inflammatory processes is thoroughly evaluated. Studies demonstrating the ability of allicin to scavenge reactive oxygen species, prevent LDL oxidation, modulate thiol-dependent redox enzymes, and enhance endogenous antioxidant systems are outlined. Additionally, the molecular pathways underlying these effects, including NF-κB, NLRP3, MAPK, Nrf2, and PPARγ/LXRα signaling, are presented. Experimental evidence suggests that allicin and/or allicin-derived organosulfur metabolites may influence atherosclerosis-related processes through coordinated regulation of lipid metabolism, oxidative stress, and inflammatory responses. Nevertheless, the interpretation of these findings remains limited by poor allicin stability, uncertain systemic exposure to intact allicin, heterogeneity among garlic formulations, and inconsistent clinical outcomes. A deeper understanding of the relative contribution of intact allicin, allicin-generating formulations, and downstream metabolites is essential to evaluate their potential as natural or adjunctive therapeutic agents. Further research into its stability, bioavailability, and optimal dosage, particularly in humans, is warranted to ensure maximal therapeutic benefit towards the prevention and/or treatment of atherosclerosis.