Effects of garlic on platelet biochemistry and physiology

Abstract

Increased platelet aggregation plays a significant role in the aetiology of cardiovascular disease, and is complex involving multiple mechanisms. On platelet activation, there is a transient increase in free cytoplasmic calcium (Ca(2+)), thromboxane A2 generation, and the activation of the fibrinogen receptor GPIIb/IIIa. Other modulators are also involved in platelet aggregation and include lipoxygenase metabolites, protein kinase C, cyclic adenosine monophosphate (cAMP), cyclic guanine monophosphate (cGMP) and nitric oxide (NO). Garlic is reported to prevent cardiovascular disease by multiple effects, one of which is the inhibition of platelet aggregation and its ability to do this has been extensively investigated in vitro, however, in vivo studies are limited. In vitro studies indicate that garlic prevents inhibition of platelet aggregation by inhibiting cyclooxygenase activity and thus thromboxane A2 formation, by suppressing mobilization of intraplatelet Ca2+, and by increasing levels of cAMP and cGMP. Garlic also displays strong antioxidant properties and activates nitric oxide synthase (NOS), leading to an increase in platelet-derived NO. It can also interact directly with the GPIIb/IIIa receptors, thus reducing the ability of platelets to bind to fibrinogen. It is concluded that garlic inhibits platelet aggregation by multiple mechanisms and may have a role in preventing cardiovascular disease.